cAMP

Medicosis Perfectionalis
14 Apr 202018:07

Summary

TLDRThe video script delves into the intricate world of cyclic AMP (cAMP) and its pivotal role in physiological processes. It distinguishes between cAMP and the antimicrobial peptide CAP, emphasizing cAMP's function as a second messenger in cellular communication. The video explains how cAMP is synthesized from ATP and its subsequent effects on various tissues, such as increasing heart rate and contractility, dilating blood vessels, and bronchi, and decreasing platelet aggregation. It also covers the mechanisms to increase cAMP levels, either by stimulating adenylate cyclase or inhibiting phosphodiesterase, and the associated therapeutic applications. The script further touches on the role of G-protein coupled receptors in cAMP regulation and the impact of different drugs on cAMP levels, highlighting the complexity and significance of this biochemistry concept in understanding medicine.

Takeaways

  • ๐Ÿงฌ Cyclic AMP (cAMP) and Cyclic GMP (cGMP) are important second messengers in cellular signaling, playing crucial roles in various physiological processes.
  • ๐Ÿ’Š The distinction between cAMP with a small 'c' (cyclic adenosine monophosphate) and CAMP with all caps (Kathelin-related antimicrobial peptide) is significant, as they have different functions.
  • ๐Ÿ“ˆ cAMP acts as a second messenger, triggered by a primary messenger such as a hormone or drug acting on a receptor, leading to a cascade of cellular responses.
  • ๐Ÿ” The level of cAMP can be increased by stimulating adenylate cyclase or inhibiting phosphodiesterase (PDE), both of which have different mechanisms and effects.
  • ๐ŸŒŸ cAMP has tissue-specific effects: in heart muscle, it increases heart rate and contractility; in blood vessels and bronchi, it leads to dilation, reducing vascular tone and systemic vascular resistance.
  • ๐Ÿšซ cAMP is degraded by phosphodiesterase (PDE), and PDE inhibitors, such as dipyridamole and sildenafil, can lead to an accumulation of cAMP and increased cellular responses.
  • ๐ŸŽฏ G-protein coupled receptors (GPCRs) play a key role in the stimulation of adenylate cyclase, with specific receptors like beta-1, beta-2, and beta-3 being coupled to cAMP production.
  • ๐Ÿ’ก Inotropic drugs like dopamine and dobutamine work by increasing cAMP levels, which in turn increase cardiac contractility through the activation of protein kinase A.
  • ๐ŸŒก๏ธ cAMP and cGMP have opposite effects on smooth muscle: cAMP leads to relaxation and dilation, while cGMP can increase contractility.
  • ๐Ÿ›ก๏ธ Phosphodiesterase inhibitors are used to manage conditions like heart failure and asthma by increasing cAMP or cGMP levels, leading to improved cardiac and bronchial function.
  • ๐Ÿ“š Understanding the complex interplay between different messengers and receptors is crucial for comprehending the sophisticated mechanisms of pharmacology and physiology.

Q & A

  • What is the difference between cAMP with the small 'c' and 'C'?

    -cAMP with the small 'c' refers to cyclic adenosine monophosphate, while cAMP with the capital 'C' refers to Kathy lo Sidon antimicrobial peptide. They are distinct molecules with different functions; the former is a second messenger involved in various cellular processes, and the latter is a part of the immune response.

  • What triggers the production of cyclic AMP (cAMP)?

    -The production of cAMP is triggered by the activation of cell surface receptors, usually by hormones, drugs, or other signaling molecules. This activation initiates a cascade that ultimately leads to the conversion of ATP to cAMP, which then acts as a second messenger in cellular signaling pathways.

  • What is the role of phosphodiesterase (PDE) in the cAMP signaling pathway?

    -Phosphodiesterase (PDE) is an enzyme that degrades cAMP, converting it into inactive products. This degradation is a critical step in turning off the cAMP signaling pathway, as it reduces the concentration of cAMP and thereby limits the duration of its effects within the cell.

  • How can cAMP levels be increased within a cell?

    -cAMP levels can be increased by either stimulating adenylate cyclase, the enzyme that produces cAMP from ATP, or by inhibiting phosphodiesterase enzymes that break down cAMP. Both approaches lead to an accumulation of cAMP, enhancing its signaling effects within the cell.

  • What are some effects of increased cAMP in different tissues?

    -Increased cAMP has tissue-specific effects. In cardiac muscle, it can increase heart rate and contractility. In smooth muscles, such as those in blood vessels and bronchi, it leads to relaxation and dilation, which can decrease vascular tone and blood pressure, and help in conditions like asthma by dilating bronchi.

  • What are some examples of phosphodiesterase inhibitors?

    -Examples of phosphodiesterase inhibitors include medications like dipyridamole, sildenafil (Viagra), and tadalafil (Cialis). These drugs inhibit PDE, leading to increased cAMP and/or cGMP levels, which can result in vasodilation, decreased platelet aggregation, and other effects depending on the specific PDE subtype targeted.

  • How do beta-agonists like dopamine and dobutamine work to increase cardiac contractility?

    -Beta-agonists like dopamine and dobutamine stimulate beta-1 adrenergic receptors, which are coupled to Gs proteins. Activation of these receptors leads to the stimulation of adenylate cyclase and the production of cAMP. Increased cAMP levels activate protein kinase A, which enhances calcium release from the sarcoplasmic reticulum, leading to increased cardiac contractility.

  • What is the role of cyclic GMP in smooth muscle relaxation?

    -Cyclic GMP plays a crucial role in smooth muscle relaxation by activating protein kinase G, which in turn stimulates phosphatases. These phosphatases remove phosphate groups from myosin light chains, leading to the deactivation of myosin and resulting in the relaxation of smooth muscles in tissues such as blood vessels and the gastrointestinal tract.

  • How do ACE inhibitors and angiotensin receptor blockers manage hypertension?

    -ACE inhibitors block the conversion of angiotensin I to angiotensin II, reducing the vasoconstriction and aldosterone release that leads to hypertension. Angiotensin receptor blockers, on the other hand, directly block the AT1 receptors that angiotensin II acts upon, preventing the vasoconstriction and sodium retention that raises blood pressure.

  • What are the potential risks of combining nitrates with PDE5 inhibitors?

    -Combining nitrates, which stimulate the production of cGMP and promote vasodilation, with PDE5 inhibitors, which also increase cGMP levels, can lead to excessive dilation of blood vessels and a severe drop in blood pressure. This combination can result in dangerous hypotension, which can be life-threatening.

  • What are some non-selective phosphodiesterase inhibitors, and what do they affect?

    -Non-selective phosphodiesterase inhibitors, such as theophylline, caffeine, and enoximone, inhibit multiple PDE subtypes, including those that break down both cAMP and cGMP. This can lead to increased levels of both second messengers, potentially causing a variety of effects such as bronchodilation, vasodilation, and increased cardiac contractility.

Outlines

00:00

๐Ÿงฌ Introduction to Cyclic AMP and its Medical Significance

This paragraph introduces the concept of cyclic AMP (cAMP) and its importance in medical science. It distinguishes between cAMP and another molecule, Kathy-lo Sidon antimicrobial peptide, and explains that cAMP is a second messenger involved in various physiological processes. The paragraph emphasizes the difference between cAMP with a lowercase 'c' (cyclic adenosine monophosphate) and 'C' (referring to the antimicrobial peptide). It also outlines the role of first and second messengers in cellular communication, where an event outside the cell triggers a cascade that ultimately leads to the production of cAMP. The paragraph further discusses the effects of cAMP on different tissues, such as increasing heart rate and contractility, dilating blood vessels, and bronchi. It also touches on how to increase cAMP levels by stimulating adenylate cyclase or inhibiting phosphodiesterase, and the implications of these actions for treating conditions like heart failure and asthma.

05:02

๐Ÿ“ˆ Functions of Cyclic AMP in Different Tissues

This paragraph delves into the specific functions of cyclic AMP (cAMP) in various tissues. It explains how cAMP acts as a second messenger to increase calcium in the heart, leading to increased heart rate and contractility. In contrast, in smooth muscle tissues, cAMP leads to relaxation, resulting in bronchodilation and vasodilation. The paragraph also discusses the role of G-protein coupled receptors (GPCRs) in stimulating adenylate cyclase and the different types of receptors involved. It further explores the effects of cAMP on lipid profiles, inflammation, and muscle proliferation, as well as its role in platelet aggregation and endothelial repair. The summary highlights the dual role of cAMP in contraction and relaxation depending on the tissue type and the importance of understanding these mechanisms for managing conditions like heart failure and hypertension.

10:03

๐Ÿ’Š Positive Inotropic Drugs and their Mechanisms

This paragraph focuses on positive inotropic drugs, which are medications that increase the force of heart muscle contractions. It explains how these drugs work by increasing cAMP or cGMP levels, leading to protein kinase A activation. The paragraph discusses the role of norepinephrine and epinephrine in the sympathetic nervous system and the adrenal medulla, and how they contribute to increased contractility. It also highlights the use of drugs like dopamine, dobutamine, and milrinone in managing heart failure by increasing cAMP levels and enhancing cardiac contractility. The summary emphasizes the importance of understanding the mechanisms of action of these drugs and their potential applications in treating cardiovascular conditions.

15:05

๐Ÿšซ Avoiding Drug Interactions and Understanding PDE Inhibitors

The final paragraph discusses the importance of avoiding certain drug combinations, particularly nitrates and sildenafil (Viagra), which can lead to severe blood vessel dilation and a dangerous drop in blood pressure. It also provides an overview of phosphodiesterase (PDE) inhibitors, which are enzymes that break down cAMP and cGMP. The paragraph explains the different subtypes of PDE inhibitors and their specific roles in boosting cAMP and cGMP levels. It mentions several PDE inhibitors, including theophylline, caffeine, and enoximone, and their non-selective nature. The summary concludes with a reminder of the importance of understanding pharmacology and the availability of educational resources for learning more about medical concepts.

Mindmap

Keywords

๐Ÿ’กCyclic AMP (cAMP)

Cyclic AMP, often referred to as cAMP, is a second messenger within cells that plays a pivotal role in various biological processes. It is synthesized from ATP and is involved in cell signaling pathways, particularly in the regulation of heart rate, blood vessel dilation, and bronchial relaxation. In the video, cAMP is highlighted as a crucial component in the physiology of the heart, bronchi, and blood vessels, affecting their function in response to various stimuli.

๐Ÿ’กPhosphodiesterase (PDE)

Phosphodiesterase, or PDE, is an enzyme that breaks down cyclic nucleotides such as cAMP and cGMP into their constituent parts. By doing so, PDE regulates the duration and intensity of the signaling pathways that involve these second messengers. In the context of the video, the inhibition of PDE leads to an accumulation of cAMP, which in turn influences the contractility of cardiac muscle and the dilation of blood vessels and bronchi, playing a significant role in the management of conditions like heart failure and asthma.

๐Ÿ’กBeta-agonists

Beta-agonists are a class of drugs that stimulate beta-adrenergic receptors, specifically beta-1 and beta-2 receptors. These receptors, when activated, lead to an increase in cAMP levels, which can enhance cardiac contractility and heart rate, as well as relax smooth muscles in the bronchi and blood vessels. In the video, beta-agonists like dopamine, dobutamine, and isoproterenol are mentioned as positive inotropic drugs that are beneficial in treating conditions like heart failure by improving heart function.

๐Ÿ’กAdenylate Cyclase

Adenylate cyclase is an enzyme that catalyzes the conversion of ATP to cAMP, thus playing a central role in the generation of this important second messenger. Its activity can be modulated by various factors, including hormones and G-protein coupled receptors. In the video, the stimulation of adenylate cyclase is discussed as a method to increase cAMP levels, which subsequently affects various physiological processes such as muscle contraction and vasodilation.

๐Ÿ’กPharmacology

Pharmacology is the branch of medicine concerned with the study of drugs and their effects on living organisms. It encompasses understanding how drugs interact with biological systems, their therapeutic uses, and the mechanisms of action. In the video, pharmacology is central to the discussion as it explains the effects of different drugs and compounds on the body's physiological processes, such as the use of phosphodiesterase inhibitors and beta-agonists in managing heart conditions.

๐Ÿ’กCardiac Myocyte

A cardiac myocyte is a specialized type of muscle cell that makes up the heart's contractile tissue. These cells are responsible for the heart's ability to pump blood throughout the body. In the video, the function of cardiac myocytes is discussed in relation to how cAMP and other signaling molecules can increase their contractility, which is crucial for maintaining effective heart function and treating conditions like heart failure.

๐Ÿ’กVasodilation

Vasodilation refers to the widening of blood vessels, which allows for increased blood flow. This physiological response is significant in reducing blood pressure and improving blood supply to various tissues. In the video, vasodilation is mentioned as one of the effects of cAMP and is particularly relevant in the context of treating hypertension and heart conditions by relaxing the smooth muscles in the blood vessel walls.

๐Ÿ’กBronchodilation

Bronchodilation is the process of opening up the bronchial tubes, which carry air to and from the lungs. This is important for improving airflow and is often a target in the treatment of respiratory conditions such as asthma. In the video, bronchodilation is discussed as a result of cAMP's action on the bronchi, which helps to alleviate the symptoms of respiratory conditions by allowing for easier breathing.

๐Ÿ’กInotropic Drugs

Inotropic drugs are medications that affect the contractility of the heart muscle. They can either increase (positive inotropic effect) or decrease (negative inotropic effect) the heart's ability to contract. In the video, inotropic drugs like dopamine and dobutamine are mentioned as agents that can enhance heart contractility, which is particularly useful in the management of heart failure.

๐Ÿ’กG-protein Coupled Receptors (GPCRs)

G-protein coupled receptors are a large family of cell surface receptors that play a key role in transmitting signals from outside the cell to the inside. When activated, they initiate a cascade of events involving second messengers like cAMP. In the video, GPCRs are discussed as they relate to the stimulation of adenylate cyclase and the subsequent increase in cAMP levels, which affects various physiological processes.

๐Ÿ’กProtein Kinase A

Protein Kinase A, or PKA, is an enzyme that phosphorylates and thereby activates or deactivates other proteins, influencing numerous cellular processes. In the video, PKA is activated by cAMP, leading to various effects on the cell, such as the regulation of heart rate and muscle contraction. PKA's activation is central to the downstream effects of cAMP signaling in different tissues, including cardiac and smooth muscle cells.

Highlights

The introduction of cyclic AMP (cAMP) as a second messenger in physiological processes.

Differentiation between cAMP (small 'c') as cyclic adenosine monophosphate and CAMP (all caps) as Kathy lo Sidon antimicrobial peptide.

Explanation of the first messenger and its role in triggering a cascade that leads to the production of cyclic AMP.

The role of adenylate cyclase in the conversion of ATP to cyclic AMP and its stimulation by Gs coupled receptors.

The mechanism by which cyclic AMP increases heart rate and contractility in cardiac muscle and leads to vasodilation and bronchodilation in blood vessels and bronchi respectively.

The function of phosphodiesterase (PDE) in the degradation of cyclic AMP and how its inhibition can lead to increased levels of cyclic AMP.

The impact of increased cyclic AMP on platelet aggregation and vasodilation, and its relevance to conditions like heart failure and asthma.

The distinction between cAMP and cGMP (cyclic guanosine monophosphate) and their respective roles in cardiac and smooth muscle tissues.

The role of inotropic drugs like dopamine and dobutamine in managing heart conditions by increasing cyclic GMP.

The importance of beta-1 adrenergic receptors in the stimulation of adenylate cyclase and the subsequent increase in cardiac contractility.

The explanation of how cyclic AMP can both increase and decrease contraction depending on the tissue type.

The process of how cyclic AMP increases 'good' cholesterol and decreases 'bad' triglycerides, and its anti-inflammatory properties.

The description of the role of cyclic AMP in the renin-angiotensin-aldosterone system and its impact on blood pressure.

The various strategies to manage hypertension, including ACE inhibitors, angiotensin receptor blockers, and calcium channel blockers.

The significance of phosphodiesterase inhibitors in treating heart failure by increasing cyclic AMP levels.

The differentiation between subtypes of phosphodiesterase enzymes and their specific roles in regulating cyclic AMP and cyclic GMP levels.

The caution against combining nitrates with PDE5 inhibitors like sildenafil due to the risk of severe hypotension.

The overview of various drugs that can increase cardiac contractility and their mechanisms of action.

Transcripts

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hey it's medicos is pure fiction

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elsewhere medicine makes perfect sense

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and today we have a pharmacology concept

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or a biochemistry concept or a

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physiology concept cyclic am Pei loved

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by your bronchi by your heart and your

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blood vessel that being said now let's

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get started when it comes to medicine

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sophistication is not an option there is

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a huge difference between CA MP with the

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C small and CA MP with Big C so in the C

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small its cyclic adenosine monophosphate

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when it's CA MP all caps this is Kathy

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lo Sidon antimicrobial peptide this is a

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second messenger these doofuses are

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polypeptides stored in the lysosome of

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the macrophages and the

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polymorphonuclear leukocytes CA MP when

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the C is small this is cyclic adenosine

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monophosphate do not confuse cyclic MP

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with v prime a MP these are not the same

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thing today's topic is cyclic MP it's a

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second messenger so where's the first

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messenger I expected that kind of

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question so look here honey second

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messenger this is the cell membrane this

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is the inside of the cell and this is

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the ECF on the inside of the cylinder

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inside of the cell membrane something

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will happen that will trigger a cascade

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and this cascade will start like this

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ATP into cyclic AMP II and cyclic AMP II

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is said to be the second messenger so

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what is the first messenger whatever the

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flip happened on the outside of the

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membrane for instance it could be a

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hormone acting on the receptor it could

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be a drug acting on the receptor it

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could be paracrine juxtacrine endocrine

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whatever something is happening to this

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receptor this is called primary

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messenger which will trigger a cascade

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called secondary messenger and then the

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cyclic AMP II will do whatever the flip

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you want it you wanted to do if this is

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a heart muscle it will increase heart

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rate and contractility if this is a

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blood vessel it will dilate the blood

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vessel if this is a bronchi it will

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dilate the bronchi so here is the story

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freakin Morning Glory ATP bye

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late cyclists become cyclic ANP and this

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is the second messenger and then by an

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enzyme called phosphodiesterase or PDE

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it will degrade and beat the living crap

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out of the cyclic GMP and converted into

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trash called degradation products cool

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so how can we increase the cyclic EMP

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it's easy

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you either stimulate adenylate cyclase

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or do you inhibit phosphodiesterase it's

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called common sense so who's gonna

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stimulate

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adenylate cyclase GS coupled receptor s

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for stimulation and by the way there's

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an eye eye for inhibition but this is

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not the today's topic

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so you either stimulate the enolate

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cyclase or you inhibit the

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phosphodiester is who's going to inhibit

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the phosphodiesterase phosphodiesterase

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inhibitors GS coupled receptors as well

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as phosphodiesterase inhibitors will

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seek to increase the level of cyclic MP

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ATP to cyclic EMP by ethylene cyclase to

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the gradation price by phosphodiester

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ace who's gonna enter the phosphodiester

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ace phosphodiesterase inhibitors can you

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give me examples yep we have medication

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she says if i read them all and see

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lastest all these are phosphodiesterase

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inhibitors when they inhibit the

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phosphorus Trace cyclic MP is gonna

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accumulate when cyclic AMP e as well as

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cyclic GMP by the way when they

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accumulate they will lead to decrease

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platelet aggregation and increase

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vasodilation and because they decrease

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platelet aggregation we have talked

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about diaper animal and Salah sizzle and

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my glorious playlist called bleeding and

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coagulation disorders so ATP to cyclic

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AMP a by phosphodiesterase degradation

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products so okay let's inhibit the

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phosphodiester ace by giving die pi read

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em all or say lost soul now nobody is

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degrading cyclic MP cyclic AMP is gonna

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accumulate into decreased platelet

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aggregation leading to increase

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vasodilation so when you increase the

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click MP inside the platelet this will

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decrease platelet aggregation when you

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increase cyclic MP or GMP inside a blood

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vessel this will decrease the vascular

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tone and you will end up with

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vasodilation these are two crucial

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functions of cyclic EMP to decrease

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platelet aggregation and to increase

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vasodilation freaky Morning Glory again

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GS coupled will stimulate a delayed

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cyclase ATP to cyclic AMP a cyclic GMP

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will activate protein kinase a how do

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you remember it everything here is a

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adenylate cyclase ATP cyclic a and P

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protein kinase a what's gonna happen

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here it depends on the tissue if you're

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talking about the heart we will increase

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calcium in the heart and this will

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increase heart rate and contractility

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especially contractility but if you're

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talking about smooth muscle tissue and

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not the heart the heart is cardiac

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muscle and we're talking smooth muscle

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right now so you will inhibit myosin

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light-chain kinase when you inhibit

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myosin light-chain kinase which was

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responsible for contraction you end up

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with it is smooth muscle relaxation so

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if you're talking about your bronchi

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bronchodilation because this is

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relaxation if you're talking about the

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vessels vasodilation because this is

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relaxation and that's why I've told you

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that cyclic MP is loved by your bronchi

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because it dilates them and it's loved

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by asthma patients because it dilates

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their bronchi what are the receptors

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that are GS coupled s for stimulation

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stimulation of what of adenylate cyclase

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you have beta 1 beta 2 and beta 3 you

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have D 1 which is dopaminergic receptors

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number 1 H 2 for histamine number 2 and

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V 2 for vasopressin mr. ADH who are the

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inhibitors who are the GI I for

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inhibition coupled receptors you have M

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2 which is muscarinic alpha 2 which is

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adrenergic and D 2 2 is inhibit or

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accept H 2 and V 2 that's just such a

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lame mnemonic

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how do inotropic drugs work they can

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work by increasing cyclic GMP because

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remember cyclic GMP and the heart muscle

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equals contraction but in the smooth

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muscle equals relaxation so let's talk

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about dopamine and dobutamine for

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example these are positive inotropic

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drugs they increase contractility so

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here is the story of your sympathetic

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nerve ending

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it gushes out norepinephrine but if

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you're talking about your adrenal

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medulla they secrete epinephrine and

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norepinephrine why didn't the

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sympathetic nerve secretes epinephrine

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because it lacks the final enzyme what

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was the name of this final enzyme it's

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called phenol if I know the mean and

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methyl transferase so you're saying that

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sympathetic does not have it yep how

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about the adrenal medulla you can bet

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there ain't money it has it it has the

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phenol ethanol I mean and methyl

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transferase and that's why the adrenal

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medulla is capable of transforming the

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norepinephrine into epinephrine that's

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why you're a dreamer Lola can secrete

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norepinephrine nerve and it can only

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secrete norepinephrine about epi semen

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is beta 1 and beta 2 beta 1 beta 2 both

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of them are GS yeah

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beta 3 as well as yes but no one cares

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about beta 3 right now

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beta 1 and beta 2 are GS GS coupled

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receptor s for stimulation let's

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stimulate the adenylate cyclase when you

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stimulate at least like this you'll

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convert ATP into cyclic MP mister second

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messenger and then cyclic EMP will lead

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to depending on the tissue if we're

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talking about the cardiac muscle

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increased contractility if you're

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talking about smooth muscle decrease

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contraction so relaxation and in smooth

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muscles of your bronchi it dilates them

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smooth muscles and your blood vessel

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again dilates them contraction the heart

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relaxation in the smooth muscles how

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about the phosphorus trace it will be

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the living crap of the cyclic GMP

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converting into trash a MP who's gonna

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inhibit the phosphorus trace three

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phosphodiesterase inhibitors such as

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diaper demo and Schloss is old but there

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is also mellow very known when you

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inhibit the degradation of cyclic MP

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what's gonna happen to the level of

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cyclic AMP it's gonna increase the in to

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increase contractility and that's the

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purpose of milrinone

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milleri known in M renown M renown they

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are all freaking the same and that's why

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milrinone dopamine and dobutamine they

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can all be used to manage CHF so here

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are all the functions of cyclic AMP e

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cyclic AMP in the places decreases play

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the degradation also through

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in Chinese a cyclic EMP can increase

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your good cholesterol it can decrease

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your triglycerides which are bad it can

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decrease inflammation decrease smooth

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muscle proliferation increase

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endothelial repair and when it comes to

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contraction it depends on the tissue I

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will increase contraction in the heart

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I will decrease contraction in the

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smooth muscle this is one of the best

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glides on the face of the earth okay

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this is your cardiac myocyte how do you

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increase contraction in increase

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contraction by calcium calcium induced

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calcium release calcium actin and myosin

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hashtag contraction where does calcium

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come from it came from a calcium channel

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in the heart okay who's gonna stimulate

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the shell mister cyclic MP through

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protein kinase a oh so how do you

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increase cardiac myocyte contractility

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you can stimulate beta 1 because beta 1

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is GS coupled and GS will stimulate mr

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adenylate cyclase when you stimulate an

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innate cyclase what's gonna happen ATP

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to cyclic AMP a cyclic am a protein

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kinase a opened the channel calcium and

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calcium induced calcium release hashtag

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contractility or you can be also smart

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by inhibiting the phosphodiester ace

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giving milrinone in Embree known amra

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known whatever you will inhibit

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phosphodiester ace

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this will increase the level of cyclic

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AMP a a.m. P ATP protein kinase a opened

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the channel in contraction that's why

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giving beta 1 agonist is a good idea for

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CSF giving memory known and ever known

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is a good idea for CSF giving calcium

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channel blockers is a stupid idea for

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CHF at least that non dihydropyridine

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calcium channel blockers your heart

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loves cyclic GMP because it increases

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heart rate and contractility your

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bronchi also love cyclic GMP because it

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dilates them Morning Glory we need you

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beta 1 beta 2 beta 3 D 1 H 2 and V 2 GS

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stimulate allayed cyclase ATP cyclic AMP

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a protein kinase a increase custom the

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heart hashtag contraction and increased

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heart rate decrease or inhibits the

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myosin light-chain kinase in smooth

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muscles hashtag relaxation relaxation of

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the bronchi relaxation of your vessels

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when you relax your vessel

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they dilate when they dilate the radius

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increases the systemic vascular

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resistance decreases and therefore your

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blood pressure decreases you're not

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convinced yet okay you dilated the

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vessel what happens to the R the radius

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it increases all happen to the systemic

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vascular resistance it will dramatically

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decrease when you dramatically decrease

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the systemic vascular resistance what's

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gonna happen to your blood pressure your

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blood pressure will go down baby and

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that's why you can give a d1 agonist

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such as Finn all the Pam to treat

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hypertension pharmacology makes perfect

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sense once you understand what the flipy

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are talking about in case there is any

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doubt beta 1 stimulation GS you know the

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rest of the story but who's gonna

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stimulate beta 1 norepinephrine

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epinephrine isoproterenol

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dopamine and dobutamine stimulate GS

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cyclic AMP a cyclic EMP will do lots of

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stuff if you're talking about the heart

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I will increase contractility if you're

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talking about the SA node I will

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increase the heart rate in the heart if

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you're talking about smooth muscles I

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will dilate smooth muscles great such as

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your bronchi and your bloodless if

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you're talking about the juxtaglomerular

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cells in the kidney i will secrete renin

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and Drennen will convert angiotensinogen

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into angiotensin one and then

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angiotensin one to angiotensin 2 by mr.

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ace and Jensen to will work on a t1

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receptor of angiotensin 2 which will

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lead to the SU constriction increase

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aldosterone release thirst sensation

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what's the function of aldosterone

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reabsorb sodium secrete potassium

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secrete hydrogen boom so you've just

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said that angiotensin 2 will work on

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this receptor and cause vasoconstriction

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and then reabsorb salt and water and

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raise my blood pressure absolutely

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so how can we manage hypertension you

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can inhibit mr. ace by giving an ACE

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inhibitor or you can inhibit the

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receptor which is a t1 receptor of

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antigens in 2 by giving and retention

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receptor blockers or you can antagonize

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the rain' by giving Alice Chiron or you

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can get calcium channel blockers why

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because they will dilate your vessels

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and they will increase cardiac

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contractility cool GS you see this GS

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by beta1 give beta-blockers yep

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or you see all of the beta 1 stimulation

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you can get it from the source

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centrally acting sympathy ola takes such

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as clonidine and alpha methyl dopa these

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are alpha-2 agonist mr. razor pain this

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is a V met inhibitor go Anitha Dean I

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call it mr. fake because it's a fake

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neurotransmitter used to fool your nerve

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ending we have talked about cyclic EMP

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let me tell you briefly about cyclic GMP

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although this is not today's topic they

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are very similar so start with gtp into

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cyclic GMP into protein kinase G will

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stimulate phosphatase phosphatase it

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will remove the phosphate to remove the

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phosphate from the myosin light-chain

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which was active and converting it into

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my supply chain without phosphate

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hashtag in active inactive myosin

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light-chain equals a relaxation in

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smooth muscles in the erectile tissue

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and in the blood vessel and that's why

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gtp and cyclic GMP will dilate your

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blood vessel hashtag relaxation how can

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i dilate my vessels easy you can give

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pro drugs of nitric oxide because nitric

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oxide will stimulate guanylate cyclase

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GTP cyclic you know the rest of the

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sweat are the products of nitric oxide

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hydrazine nitroprusside nitrates and

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these will stimulate granade cyclase and

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relax your smooth muscle and dilate your

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vessels brilliant is there another way

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of course you can inhibit phosphodiester

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ace 5 which will inhibit the conversion

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of cyclic GMP into GMP and this will

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increase cyclic GMP to relax your blood

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vessels and relax your erectile tissue

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what are these drugs so then FL 2 denna

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Phil for Dana Ville okay so I either

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give one of these or one of these to

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relax my smooth muscles excellent should

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you combine both together this is known

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as crazy because both of them have the

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same function if you combine them

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together this will lead to severe

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dilation of blood vessels and severe

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drop in blood pressure you can die of

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hypotension

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so never ever ever combine nitrates with

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sildenafil aka viagra I'm an old

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dinosaur who remember

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when viagra was invented and Starbucks

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introduced viagra Chino one cup and you

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will be up all night you remember when I

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told you about the calcium channel in

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your heart which is responsible for

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increasing cardiac contractile - yes

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this is called the l-type calcium

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channel responsible calcium induced

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calcium release from the sarcoplasmic

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reticulum which is a smooth endoplasmic

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reticulum what are the drugs that can

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boost my contractility dopamine

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dobutamine epinephrine norepinephrine

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isoproterenol last thing the

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phosphodiesterase inhibitors by the way

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the same enzyme phosphatase is

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responsible for breaking down cyclic MP

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or cyclic GMP however there are many

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many many subtypes of this phosphorus

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trace we have phosphodiester ace 4 7 & 8

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and they specialize in boosting cyclic

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EMP by preventing its degradation we

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have other types of phosphodiester aces

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5 6 & 9 and they specialized for cyclic

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GMP they will boost it by inhibiting its

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degradation and we have other numbers

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such as phosphorus reached one two three

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ten and eleven and they specialize in

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both cyclic GMP and cyclic GMP let me

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give you some drugs how about

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theophylline caffeine Emmy no foolin

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missile anthem these are non selective

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phosphodiesterase inhibitors cool so

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then if n is pde5 where is five here

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here and that's why it's specialized in

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cyclic GMP type I rhythm ol is three so

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lost is always three never known are

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three and that's why they can specialize

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in cyclic MP and or cyclic GMP cyclic

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AMP II in a nutshell I will increase

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your good cholesterol

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I'll decrease your bad triglycerides LD

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crease inflammation and smooth muscle

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proliferation I will repair your indicia

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me and will inhibit your platelet

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aggregation which will help you in

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deuterium this will make your

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endothelium happy when it comes to

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contraction it depends on the tissue if

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you're talking about cardiac muscle I

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will boost contraction if you're talking

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about smoother muscles I will decrease

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contraction if you're starting to like

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form ecology for the first time ever I

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have antibiotics course on my website

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medical says perfection as calm as will

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as a cardiac form ecology course on my

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website

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fifty videos for cardiac form ecology

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and forty videos for antibiotics ninety

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videos in total and

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you can kiss antibiotics and Kotick for

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ecology goodbye forever these two

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courses are on sale right now they are

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the cheapest they have ever been

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thank you so much for watching don't

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forget to subscribe hit the bell and

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click on the join button you can support

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me here or here don't forget to get my

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card it form ecology course and my

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antibiotics course at medicos is

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perfectionist calm thank you so much for

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watching as always be safe stay happy

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and study hard

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this is medicos is perfection arrows

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where medicine makes perfect sense

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Related Tags
PharmacologyPhysiologyCyclic AMPHeart FunctionBlood VesselsPlatelet AggregationPhosphodiesterase InhibitorsCardiac MyocyteSmooth MuscleMedical Education