cAMP
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
- 𧬠Cyclic AMP (cAMP) and Cyclic GMP (cGMP) are important second messengers in cellular signaling, playing crucial roles in various physiological processes.
- π 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.
- π 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.
- π The level of cAMP can be increased by stimulating adenylate cyclase or inhibiting phosphodiesterase (PDE), both of which have different mechanisms and effects.
- π 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.
- π« 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.
- π― 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.
- π‘ Inotropic drugs like dopamine and dobutamine work by increasing cAMP levels, which in turn increase cardiac contractility through the activation of protein kinase A.
- π‘οΈ cAMP and cGMP have opposite effects on smooth muscle: cAMP leads to relaxation and dilation, while cGMP can increase contractility.
- π‘οΈ 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.
- π 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
𧬠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.
π 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.
π 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.
π« 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
π‘Cyclic AMP (cAMP)
π‘Phosphodiesterase (PDE)
π‘Beta-agonists
π‘Adenylate Cyclase
π‘Pharmacology
π‘Cardiac Myocyte
π‘Vasodilation
π‘Bronchodilation
π‘Inotropic Drugs
π‘G-protein Coupled Receptors (GPCRs)
π‘Protein Kinase A
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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