cAMP

Summary

The 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

• 🧬 Cyclic AMP (cAMP) and Cyclic GMP (cGMP) are important second messengers in cellular signaling, playing crucial roles in various physiological processes.
• 💊 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.
• 📈 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.
• 🔍 The level of cAMP can be increased by stimulating adenylate cyclase or inhibiting phosphodiesterase (PDE), both of which have different mechanisms and effects.
• 🌟 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.
• 🚫 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.
• 🎯 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.
• 💡 Inotropic drugs like dopamine and dobutamine work by increasing cAMP levels, which in turn increase cardiac contractility through the activation of protein kinase A.
• 🌡️ cAMP and cGMP have opposite effects on smooth muscle: cAMP leads to relaxation and dilation, while cGMP can increase contractility.
• 🛡️ 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.
• 📚 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

🧬 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

📈 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

💊 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

🚫 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.

Keywords

💡Cyclic 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.

💡Phosphodiesterase (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.

💡Beta-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.

💡Adenylate 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.

💡Pharmacology

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.

💡Cardiac 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.

💡Vasodilation

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.

💡Bronchodilation

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.

💡Inotropic 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.

💡G-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.

💡Protein 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

hey it's medicos is pure fiction

elsewhere medicine makes perfect sense

and today we have a pharmacology concept

or a biochemistry concept or a

physiology concept cyclic am Pei loved

by your bronchi by your heart and your

blood vessel that being said now let's

get started when it comes to medicine

sophistication is not an option there is

a huge difference between CA MP with the

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

small its cyclic adenosine monophosphate

when it's CA MP all caps this is Kathy

lo Sidon antimicrobial peptide this is a

second messenger these doofuses are

polypeptides stored in the lysosome of

the macrophages and the

polymorphonuclear leukocytes CA MP when

the C is small this is cyclic adenosine

monophosphate do not confuse cyclic MP

with v prime a MP these are not the same

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

second messenger so where's the first

messenger I expected that kind of

question so look here honey second

messenger this is the cell membrane this

is the inside of the cell and this is

the ECF on the inside of the cylinder

inside of the cell membrane something

will happen that will trigger a cascade

and this cascade will start like this

ATP into cyclic AMP II and cyclic AMP II

is said to be the second messenger so

what is the first messenger whatever the

flip happened on the outside of the

membrane for instance it could be a

hormone acting on the receptor it could

be a drug acting on the receptor it

could be paracrine juxtacrine endocrine

whatever something is happening to this

receptor this is called primary

messenger which will trigger a cascade

called secondary messenger and then the

cyclic AMP II will do whatever the flip

you want it you wanted to do if this is

a heart muscle it will increase heart

rate and contractility if this is a

blood vessel it will dilate the blood

vessel if this is a bronchi it will

dilate the bronchi so here is the story

freakin Morning Glory ATP bye

late cyclists become cyclic ANP and this

is the second messenger and then by an

enzyme called phosphodiesterase or PDE

it will degrade and beat the living crap

out of the cyclic GMP and converted into

trash called degradation products cool

so how can we increase the cyclic EMP

it's easy

you either stimulate adenylate cyclase

or do you inhibit phosphodiesterase it's

called common sense so who's gonna

stimulate

adenylate cyclase GS coupled receptor s

for stimulation and by the way there's

an eye eye for inhibition but this is

not the today's topic

so you either stimulate the enolate

cyclase or you inhibit the

phosphodiester is who's going to inhibit

the phosphodiesterase phosphodiesterase

inhibitors GS coupled receptors as well

as phosphodiesterase inhibitors will

seek to increase the level of cyclic MP

ATP to cyclic EMP by ethylene cyclase to

the gradation price by phosphodiester

ace who's gonna enter the phosphodiester

ace phosphodiesterase inhibitors can you

give me examples yep we have medication

she says if i read them all and see

lastest all these are phosphodiesterase

inhibitors when they inhibit the

phosphorus Trace cyclic MP is gonna

accumulate when cyclic AMP e as well as

cyclic GMP by the way when they

accumulate they will lead to decrease

platelet aggregation and increase

vasodilation and because they decrease

platelet aggregation we have talked

about diaper animal and Salah sizzle and

my glorious playlist called bleeding and

coagulation disorders so ATP to cyclic

AMP a by phosphodiesterase degradation

products so okay let's inhibit the

phosphodiester ace by giving die pi read

em all or say lost soul now nobody is

degrading cyclic MP cyclic AMP is gonna

accumulate into decreased platelet

aggregation leading to increase

vasodilation so when you increase the

click MP inside the platelet this will

decrease platelet aggregation when you

increase cyclic MP or GMP inside a blood

vessel this will decrease the vascular

tone and you will end up with

vasodilation these are two crucial

functions of cyclic EMP to decrease

platelet aggregation and to increase

vasodilation freaky Morning Glory again

GS coupled will stimulate a delayed

cyclase ATP to cyclic AMP a cyclic GMP

will activate protein kinase a how do

you remember it everything here is a

adenylate cyclase ATP cyclic a and P

protein kinase a what's gonna happen

here it depends on the tissue if you're

talking about the heart we will increase

calcium in the heart and this will

increase heart rate and contractility

especially contractility but if you're

talking about smooth muscle tissue and

not the heart the heart is cardiac

muscle and we're talking smooth muscle

right now so you will inhibit myosin

light-chain kinase when you inhibit

myosin light-chain kinase which was

responsible for contraction you end up

with it is smooth muscle relaxation so

if you're talking about your bronchi

bronchodilation because this is

relaxation if you're talking about the

vessels vasodilation because this is

relaxation and that's why I've told you

that cyclic MP is loved by your bronchi

because it dilates them and it's loved

by asthma patients because it dilates

their bronchi what are the receptors

that are GS coupled s for stimulation

stimulation of what of adenylate cyclase

you have beta 1 beta 2 and beta 3 you

have D 1 which is dopaminergic receptors

number 1 H 2 for histamine number 2 and

V 2 for vasopressin mr. ADH who are the

inhibitors who are the GI I for

inhibition coupled receptors you have M

2 which is muscarinic alpha 2 which is

adrenergic and D 2 2 is inhibit or

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

lame mnemonic

how do inotropic drugs work they can

work by increasing cyclic GMP because

remember cyclic GMP and the heart muscle

equals contraction but in the smooth

muscle equals relaxation so let's talk

about dopamine and dobutamine for

example these are positive inotropic

drugs they increase contractility so

here is the story of your sympathetic

nerve ending

it gushes out norepinephrine but if

you're talking about your adrenal

medulla they secrete epinephrine and

norepinephrine why didn't the

sympathetic nerve secretes epinephrine

because it lacks the final enzyme what

was the name of this final enzyme it's

called phenol if I know the mean and

methyl transferase so you're saying that

sympathetic does not have it yep how

about the adrenal medulla you can bet

there ain't money it has it it has the

phenol ethanol I mean and methyl

transferase and that's why the adrenal

medulla is capable of transforming the

norepinephrine into epinephrine that's

why you're a dreamer Lola can secrete

norepinephrine nerve and it can only

secrete norepinephrine about epi semen

is beta 1 and beta 2 beta 1 beta 2 both

of them are GS yeah

beta 3 as well as yes but no one cares

about beta 3 right now

beta 1 and beta 2 are GS GS coupled

receptor s for stimulation let's

stimulate the adenylate cyclase when you

stimulate at least like this you'll

convert ATP into cyclic MP mister second

messenger and then cyclic EMP will lead

to depending on the tissue if we're

talking about the cardiac muscle

increased contractility if you're

talking about smooth muscle decrease

contraction so relaxation and in smooth

muscles of your bronchi it dilates them

smooth muscles and your blood vessel

again dilates them contraction the heart

relaxation in the smooth muscles how

about the phosphorus trace it will be

the living crap of the cyclic GMP

converting into trash a MP who's gonna

inhibit the phosphorus trace three

phosphodiesterase inhibitors such as

diaper demo and Schloss is old but there

is also mellow very known when you

inhibit the degradation of cyclic MP

what's gonna happen to the level of

cyclic AMP it's gonna increase the in to

increase contractility and that's the

purpose of milrinone

milleri known in M renown M renown they

are all freaking the same and that's why

milrinone dopamine and dobutamine they

can all be used to manage CHF so here

are all the functions of cyclic AMP e

cyclic AMP in the places decreases play

the degradation also through

in Chinese a cyclic EMP can increase

your good cholesterol it can decrease

your triglycerides which are bad it can

decrease inflammation decrease smooth

muscle proliferation increase

endothelial repair and when it comes to

contraction it depends on the tissue I

will increase contraction in the heart

I will decrease contraction in the

smooth muscle this is one of the best

glides on the face of the earth okay

this is your cardiac myocyte how do you

increase contraction in increase

contraction by calcium calcium induced

calcium release calcium actin and myosin

hashtag contraction where does calcium

come from it came from a calcium channel

in the heart okay who's gonna stimulate

the shell mister cyclic MP through

protein kinase a oh so how do you

increase cardiac myocyte contractility

you can stimulate beta 1 because beta 1

is GS coupled and GS will stimulate mr

adenylate cyclase when you stimulate an

innate cyclase what's gonna happen ATP

to cyclic AMP a cyclic am a protein

kinase a opened the channel calcium and

calcium induced calcium release hashtag

contractility or you can be also smart

by inhibiting the phosphodiester ace

giving milrinone in Embree known amra

known whatever you will inhibit

phosphodiester ace

this will increase the level of cyclic

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

the channel in contraction that's why

giving beta 1 agonist is a good idea for

CSF giving memory known and ever known

is a good idea for CSF giving calcium

channel blockers is a stupid idea for

CHF at least that non dihydropyridine

calcium channel blockers your heart

loves cyclic GMP because it increases

heart rate and contractility your

bronchi also love cyclic GMP because it

dilates them Morning Glory we need you

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

stimulate allayed cyclase ATP cyclic AMP

a protein kinase a increase custom the

heart hashtag contraction and increased

heart rate decrease or inhibits the

myosin light-chain kinase in smooth

muscles hashtag relaxation relaxation of

the bronchi relaxation of your vessels

when you relax your vessel

they dilate when they dilate the radius

increases the systemic vascular

resistance decreases and therefore your

blood pressure decreases you're not

convinced yet okay you dilated the

vessel what happens to the R the radius

it increases all happen to the systemic

vascular resistance it will dramatically

decrease when you dramatically decrease

the systemic vascular resistance what's

gonna happen to your blood pressure your

blood pressure will go down baby and

that's why you can give a d1 agonist

such as Finn all the Pam to treat

hypertension pharmacology makes perfect

sense once you understand what the flipy

are talking about in case there is any

doubt beta 1 stimulation GS you know the

rest of the story but who's gonna

stimulate beta 1 norepinephrine

epinephrine isoproterenol

dopamine and dobutamine stimulate GS

cyclic AMP a cyclic EMP will do lots of

stuff if you're talking about the heart

I will increase contractility if you're

talking about the SA node I will

increase the heart rate in the heart if

you're talking about smooth muscles I

will dilate smooth muscles great such as

your bronchi and your bloodless if

you're talking about the juxtaglomerular

cells in the kidney i will secrete renin

and Drennen will convert angiotensinogen

into angiotensin one and then

angiotensin one to angiotensin 2 by mr.

ace and Jensen to will work on a t1

receptor of angiotensin 2 which will

lead to the SU constriction increase

aldosterone release thirst sensation

what's the function of aldosterone

reabsorb sodium secrete potassium

secrete hydrogen boom so you've just

said that angiotensin 2 will work on

this receptor and cause vasoconstriction

and then reabsorb salt and water and

raise my blood pressure absolutely

so how can we manage hypertension you

can inhibit mr. ace by giving an ACE

inhibitor or you can inhibit the

receptor which is a t1 receptor of

antigens in 2 by giving and retention

receptor blockers or you can antagonize

the rain' by giving Alice Chiron or you

can get calcium channel blockers why

because they will dilate your vessels

and they will increase cardiac

contractility cool GS you see this GS

by beta1 give beta-blockers yep

or you see all of the beta 1 stimulation

you can get it from the source

centrally acting sympathy ola takes such

as clonidine and alpha methyl dopa these

are alpha-2 agonist mr. razor pain this

is a V met inhibitor go Anitha Dean I

call it mr. fake because it's a fake

neurotransmitter used to fool your nerve

ending we have talked about cyclic EMP

let me tell you briefly about cyclic GMP

although this is not today's topic they

are very similar so start with gtp into

cyclic GMP into protein kinase G will

stimulate phosphatase phosphatase it

will remove the phosphate to remove the

phosphate from the myosin light-chain

which was active and converting it into

my supply chain without phosphate

hashtag in active inactive myosin

light-chain equals a relaxation in

smooth muscles in the erectile tissue

and in the blood vessel and that's why

gtp and cyclic GMP will dilate your

blood vessel hashtag relaxation how can

i dilate my vessels easy you can give

pro drugs of nitric oxide because nitric

oxide will stimulate guanylate cyclase

GTP cyclic you know the rest of the

sweat are the products of nitric oxide

hydrazine nitroprusside nitrates and

these will stimulate granade cyclase and

relax your smooth muscle and dilate your

vessels brilliant is there another way

of course you can inhibit phosphodiester

ace 5 which will inhibit the conversion

of cyclic GMP into GMP and this will

increase cyclic GMP to relax your blood

vessels and relax your erectile tissue

what are these drugs so then FL 2 denna

Phil for Dana Ville okay so I either

give one of these or one of these to

relax my smooth muscles excellent should

you combine both together this is known

as crazy because both of them have the

same function if you combine them

together this will lead to severe

dilation of blood vessels and severe

drop in blood pressure you can die of

hypotension

so never ever ever combine nitrates with

sildenafil aka viagra I'm an old

dinosaur who remember

when viagra was invented and Starbucks

introduced viagra Chino one cup and you

will be up all night you remember when I

told you about the calcium channel in

your heart which is responsible for

increasing cardiac contractile - yes

this is called the l-type calcium

channel responsible calcium induced

calcium release from the sarcoplasmic

reticulum which is a smooth endoplasmic

reticulum what are the drugs that can

boost my contractility dopamine

dobutamine epinephrine norepinephrine

isoproterenol last thing the

phosphodiesterase inhibitors by the way

the same enzyme phosphatase is

responsible for breaking down cyclic MP

or cyclic GMP however there are many

many many subtypes of this phosphorus

trace we have phosphodiester ace 4 7 & 8

and they specialize in boosting cyclic

EMP by preventing its degradation we

have other types of phosphodiester aces

5 6 & 9 and they specialized for cyclic

GMP they will boost it by inhibiting its

degradation and we have other numbers

such as phosphorus reached one two three

ten and eleven and they specialize in

both cyclic GMP and cyclic GMP let me

give you some drugs how about

theophylline caffeine Emmy no foolin

missile anthem these are non selective

phosphodiesterase inhibitors cool so

then if n is pde5 where is five here

here and that's why it's specialized in

cyclic GMP type I rhythm ol is three so

lost is always three never known are

three and that's why they can specialize

in cyclic MP and or cyclic GMP cyclic

AMP II in a nutshell I will increase

your good cholesterol

I'll decrease your bad triglycerides LD

crease inflammation and smooth muscle

proliferation I will repair your indicia

me and will inhibit your platelet

aggregation which will help you in

deuterium this will make your

endothelium happy when it comes to

contraction it depends on the tissue if

you're talking about cardiac muscle I

will boost contraction if you're talking

about smoother muscles I will decrease

contraction if you're starting to like

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perfectionist calm thank you so much for

watching as always be safe stay happy

and study hard

this is medicos is perfection arrows

where medicine makes perfect sense