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CVPR > Unit 1 - regulation > Flashcards

Unit 1 - regulation Flashcards

1
Q

How does sympathetic nervous system stimulation increase inotropy

A 
Beta-1 receptors --> Gs --> cAMP --> PKA
PKA phosphorylates
1. L-Type calcium channels (DHPR)
2. RyR Receptors of SR
3. PLB = Phospholambam
4. TP-I (luistropy)
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2
Q

So in follow up, why would a beta-adrenergic receptor antagonist decrease heart contractile force?

A
  1. decreased ca2+ influx from L-type –> decrease for storage
  2. decrease RyR receptor sensitivity - decrease release
  3. decrease PLB-p –> more inhibition of SERCA
  4. decrease TP-I-p –> reduced cycle velocity
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3
Q

How does sympathetic activation lead to increased chronotropy?

A

Beta-1 receptors –> Gs –> cAMP –> PKA
cAMP directly binds If (HCN) channel
-increasing likelihood of opening (raise resting)
PKA phosphorylates
- L-type channel and RyR which both act to increase intracellular calcium
Increased intracellular calcium causes the NCX exchanger to pump out 1 Ca2+ for pumping in 3Nat+

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4
Q

So in follow up, why would a beta adrenergic receptor antagonist decrease heart rate?

A

It would inhibit the production of cAMP and thus prevent increased opening of If

I would inhibit the production of PKA and thus prevent the elevated intracellular Ca2+ that enables the NCX to enable depolarization

Now recall the If is for pacers, not makers

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5
Q

How does the parasympathetic nervous system decrease chronotropy?

A

Acetylcholine binds to muscarinic acetylcholine receptors (M2) which are the G coupled ones (Gi/o)

The Gi inhibits adenyl cyclase from making cAMP so the funny current can flow as easily
cAMP can’t activate PKA
PKA can’t phosphorylate it’s targets (Ca-L, Ryr)
Intracellular Calcium is not as easily elevated –> NCX not as active

IN ADDITION
G-by subunit opens GIRK - the g-couple inward potassium rectifier - which further increases outward K+ (hyperpolarizes)

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6
Q

what is the primary mechanism for parasympathetic control of chronotropy?

A

Activation of GIRK via M2 G-ay

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7
Q

How many nuclei are in VSMC?

A

1

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8
Q

Do vascular smooth muscle cells have sarcomeres?

A

no, the contractile units in smooth muscle are not organized into sarcomeres - however, they are still comprised of actin and myosin - just not organized

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9
Q

Do vascular smooth muscle cells have troponin / tropomyosin

A

no, they do not have and are not regulated by troponin / tropomyosin - which surround the thin filament in striated muscle - rarher vascular smooth muscle cells are regulated via myosin light chain

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10
Q

Do vascular myocytes require SR Ca2+ release for contraction?

A

No

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11
Q

how are smooth muscle cells’ contractile properties regulated?

A

via phosphorylation of myosin light chain via myosin light chain kinase which is activated by calcium-calmodulin

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12
Q

How does cAMP influence smooth muscle cell contracility

A

ACTUALLY - cAMP inhibits myosin light chain kinase and thus, prevent contraction

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13
Q

How is contraction halted in smooth muscle cells?

A

when myosin light chain is dephosphorylated by myosin light chain phosphatase

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14
Q

adranergic targets on vascular smooth muscle cells?

! NOTABLE UNIQUE QUALITY OF SKELETALE MUSCLE?!

A

alpha receptors!

alpha receptors activate Gq –> cleaves phosphotidylinosotol –> IP3/DAG –> IP3 can then increase cytosolic Ca2+ via receptors on SR–> bind calmodulin –> MLCK –> vasoconstriction

Unique skeletal muscle targets - beta-2 receptors - which activate Gs and cause increase cAMP via adenyl cyclase activation –> inhibits MLCK –> vasodilation

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15
Q

decrease sympathetic tone on heart?

A

cause decreased heart rate and inotropy

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16
Q

decrease sympathetic tone on vasculature?

A

increase in vasodilation

17
Q

baroreceptor reflex response to increases in blood pressure?

A

sense increase pressure in aortic arch and carotid sinus –> increase firing –> decrease sympathetic and increase parasympathetic tone

18
Q

what is the primary mechanism of the body to match the blood it gets with the blood it needs?

A

via vasoactive metabolites

19
Q

what are 4 metabolites that influence peripheral vasculature? cause it it dilate?

A

low O2
High CO2 (low pH)
High K+
High adenosine

20
Q

via what mechanism does adenosine increase vasodilation?

A

it binds A2 purinergic receptors of vascular smooth muscle (GPCR) - increasing cAMP

Recall cAMP has inhibitory effect in VSMC inhibiting MLCK and thus vasodilating

21
Q

myogenic response of VSMC?

A

In response to being stretched, the vascular smooth muscle cells will contract! (via activation of Trp non-selective Ca2+ channels)

Thus if if the flow is excessive, their contraction will lower it

22
Q

endothelail mediated regulation of vasculature

what causes dilation
what cause contraction

A 
NO = potent vasodilator
Endothelin = potent vasoconstrictor
  • both these mediators are produced in the endothelial cells and then effect the VSMCs
23
Q

what is the primary mechanism for long term control of blood pressure?

A

RAA- system

24
Q

Angiotensin II direct effects?

A

systemic vasoconstriction via GPCRs of VSMCs (must increase cAMP)

25
Q

Angiotensin II indirect effects?

A

sympathetic stimulation
aldosterone release
endothelin release
ADH release

26
Q

Aldosterone effect?

A

promotes Na+ resorption in kidney collecting duct (K+ secretion)

27
Q

So… spironolactone competes for aldosterone receptors, what effects would it have?

A

inhibits aldosterone sensitive Na+ resorption in kidney collecting duct - here if we don’t resorb sodium we don’t dump K+

so potassium sparing diuretic
also aids in inhibiting heart remodeling

28
Q

ADH effects?

A

increased water resorption in collecting duct

can cause vasoconstriction

29
Q

where and how do thiazide diuretics (e.g.chlorothiazide) act?

A

distal convoluted tubule

block Na+Cl- channel –> blocking Na+ resorption

30
Q

consequence of thiazeide (e.g. chlorothiazide) site of action?

A

increased Na+ delivery (in lumen) to collecting duct –> more K+ exchange –> hypokalemia possible

31
Q

pre-requisite for thiazide diuretics?

A

normal GFR

not hypokalemic :)

32
Q

What is atrial natriuretic peptide?

major effects? (3)

A

peptide hormone released in response to atrial stretch
vasodilation
natriuresis (+ diuresis)
inhibit renin and aldosterone release

33
Q

ANP moa of vasodilation

A

receptor binding –> cGMP –> cGMP activates SERCA

CVPR (2 decks)

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