10. Vascular Signaling (Reg CV System) Flashcards Preview

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Flashcards in 10. Vascular Signaling (Reg CV System) Deck (62):
1

What is the mygogenic response?

an intrinsic feedback mechanism to maintain constant flow despite changes in pressure; causes constriction

2

What does myogenic response counteract?

increased pressure

3

The myogenic response can be overcome by ____.

vasoactive metabolites

4

Give an example of when the myogenic response might kick in.

when you quickly stand up

5

What channels cause the myogenic response?

stretch-activated ion channels of the Trp family

6

Stretch-activated ion channels of the Trp family cause what?

the myogenic response

7

What produces NO?

vascular endothelium via nitric oxide synthase

8

What does NO do?

causes vasodilation

9

Basal NO release helps to set the _____.

resting vascular tone

10

A decrease in NO is one factor associated with risk of _____.

atherosclerosis

11

What enzyme is sensitive to cigarette smoke, increasing risk of CVD?

nitric oxide synthase

12

Nitric oxide synthase (NOS) produces NO from ____.

L-arginine and O2

13

What does NO activate?

guanylyl cyclase, to produce cGMP

14

What in the blood stimulates production of NO?

humoral agents, like bradykinin and ACh

15

Humoral agents cause _____, which activates nitric oxide synthase (NOS).

an increase in intracellular Ca++

16

1. NO activates guanylyl cyclase to produce cGMP
2. cGMP activates ____
3. PKG reduces intracellular Ca++ via activation of SERCA and inhibition of L-type Ca++ channels
4. Decreased Ca++ causes vasodilation via reduced MLCK activity

PKG

17

1. NO activates guanylyl cyclase to produce cGMP
2. cGMP activates PKG
3. PKG _____ via activation of SERCA and inhibition of L-type Ca++ channels
4. Decreased Ca++ causes vasodilation via reduced MLCK activity

1. NO activates guanylyl cyclase to produce cGMP
2. cGMP activates ____
3. PKG reduces intracellular Ca++ via activation of SERCA and inhibition of L-type Ca++ channels
4. Decreased Ca++ causes vasodilation via reduced MLCK activity

18

1. NO activates guanylyl cyclase to produce cGMP
2. cGMP activates PKG
3. PKG reduces intracellular Ca++ via activation of ____ and inhibition of _____
4. Decreased Ca++ causes vasodilation via reduced MLCK activity

SERCA; L-type Ca++ channels

19

1. NO activates guanylyl cyclase to produce cGMP
2. cGMP activates PKG
3. PKG reduces intracellular Ca++ via activation of SERCA and inhibition of L-type Ca++ channels
4. Decreased Ca++ causes _____ via reduced MLCK activity

vasodilation

20

1. NO activates guanylyl cyclase to produce cGMP
2. cGMP activates PKG
3. PKG reduces intracellular Ca++ via activation of SERCA and inhibition of L-type Ca++ channels
4. Decreased Ca++ causes vasodilation via _____

reduced MLCK activity

21

1. NO activates guanylyl cyclase to produce cGMP
2. cGMP activates PKG
3. PKG reduces intracellular Ca++ via activation of SERCA and inhibition of L-type Ca++ channels
4. Decreased Ca++ causes vasodilation via reduced MLCK activity

NO action in vascular smooth muscle cells (VSMCs)

22

Where is endothelin produced?

by the vascular endothelium

23

What is endothelin?

a peptide that causes vasoconstriction

24

What inhibits endothelin?

vasodilators like NO and ANP

25

What stimulates endothelin?

vasoconstrictors such as angiotensin, ADH, thrombin

26

After endothelin is released, where does it bind?

to ET receptors (a type of GPCR)

27

What is the natural counterpart of NO?

endothelin

28

What organ is responsible for regulation of BP?

the kidney

29

_____ is the 1a system for long-term control of BP.

The RAAS

30

What to renal juxtaglomerular cells produce?

renin and angiotensin

31

Where are renin and angiotensin produced?

by the renal juxtaglomerular cells

32

What stimulates renin and angiotensin production?

sympathetic stimulation
decreased BP
decreases Na+ absorption

33

What do....
sympathetic stimulation
decreased BP
decreases Na+ absorption
....cause?

production of renin and angiotensin

34

____ cleaves inactive angiotensinogen into angiotensin I (AI), which is also inactive.

Renin

35

Renin cleaves inactive _____ into angiotensin I (AI), which is also inactive.

angiotensinogen

36

Renin cleaves inactive angiotensinogen into _____, which is also inactive.

angiotensin I (AI)

37

____ is cleaved by Angiotensin Converting Enzyme (ACE) to Angiotensin II (AII), which is a vasoconstrictor.

Angiotensin I

38

Angiotensin I is cleaved by _____ to Angiotensin II (AII), which is a vasoconstrictor.

Angiotensin Converting Enzyme (ACE)

39

Angiotensin I is cleaved by Angiotensin Converting Enzyme (ACE) to _____, which is a vasoconstrictor.

Angiotensin II (AII)

40

What are ACE inhibitors and angiotensin II receptor blockers?

tx for HTN and HF

41

What is the direct affect of angiotensin II?

causes vasoconstriction by binding to GPCRs

42

What is the indirect affect of angiotensin II?

stimulates SNS activity and the release of aldosterone, endothelin, and ADH

43

What is aldosterone?

a steroid hormone produced by the adrenal cortex

44

What does aldosterone do?

it promotes Na and water in the collecting duct = re-absorption to increase blood volume and BP

45

What is ADH?

a peptide hormone formed in the hypothalamus (released by pituitary)

46

What stimulates ADH release?

hypovolemia
hypotension
high osmolarity
angiotensin II
SNS

47

ADH can also cause ____ when it binds to blood vasculature receptors.

vasoconstriction

48

What is the purpose of the RAAS system?

to increase BP and blood volume

49

What is atrial natriuretic peptide (ANP)?

a peptide produced by the atria in response to stretch that causes vasodilation

50

What does natriuretic mean?

sodium excreting

51

What does ANP bind to?

natriuretic peptide receptors, not GPCRs, to produce cGMP

52

What are cGMP's affects?

activates SERCA, stimulates Ca++ uptake

53

ANP increases the _____ and secretion of ____ and ____.

glomerular filtration rate; Na, water

54

In vasculature, ANP is a ____ because it inhibits endothelin release. In the adrenal gland, it inhibits the release of ____ and ____.

vasodilator; aldosterone and renin

55

What are the immediate effects of standing?

1. R atrial pressure drops
2. venous pressure in the legs increases

56

What is orthostatic hypertension?

fainting or lightheadedness upon standing bc of compromised baroreceptor reflex or already low BP

57

When is the effect of orthostatic hypertension more pronounced?

in warm weather bc of vasodilation in the skin

58

Anticipation of exercise increases _____ tone and
decreases _____ activity to increase heart rate and inotropy, thereby increasing cardiac output. What is this mechanism called?

sympathetic; parasympathetic; the central command mechanism

59

What is the central command mechanism?

Anticipation of exercise increases sympathetic and
decreases parasympathetic activity to increase heart
rate and inotropy, thereby increasing cardiac output.

60

Activity of skeletal muscles increases venous return,
which increases _____ via the Frank-Starling mechanism.

stroke volume

61

Activity of skeletal muscles increases venous return,
which increases stroke volume via the _____ mechanism.

Frank-Starling

62

In the exercising muscles, ______ dilate arterioles to increase blood flow (remember Pouiseulle’s Law, r^4).

vasoactive metabolites