Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

CVPR Exam I > 10. Vascular Signaling (Reg CV System) > Flashcards

10. Vascular Signaling (Reg CV System) Flashcards

1
Q

What is the mygogenic response?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What does myogenic response counteract?

A

increased pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

The myogenic response can be overcome by ____.

A

vasoactive metabolites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

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

A

when you quickly stand up

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What channels cause the myogenic response?

A

stretch-activated ion channels of the Trp family

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

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

A

the myogenic response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What produces NO?

A

vascular endothelium via nitric oxide synthase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What does NO do?

A

causes vasodilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Basal NO release helps to set the _____.

A

resting vascular tone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

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

A

atherosclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

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

A

nitric oxide synthase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Nitric oxide synthase (NOS) produces NO from ____.

A

L-arginine and O2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What does NO activate?

A

guanylyl cyclase, to produce cGMP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What in the blood stimulates production of NO?

A

humoral agents, like bradykinin and ACh

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

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

A

an increase in intracellular Ca++

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q
  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
A

PKG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q
  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
A
  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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q
  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
A

SERCA; L-type Ca++ channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q
  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
A

vasodilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q
  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 _____
A

reduced MLCK activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q
  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
A

NO action in vascular smooth muscle cells (VSMCs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Where is endothelin produced?

A

by the vascular endothelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is endothelin?

A

a peptide that causes vasoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What inhibits endothelin?

A

vasodilators like NO and ANP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What stimulates endothelin?

A

vasoconstrictors such as angiotensin, ADH, thrombin

26
Q

After endothelin is released, where does it bind?

A

to ET receptors (a type of GPCR)

27
Q

What is the natural counterpart of NO?

A

endothelin

28
Q

What organ is responsible for regulation of BP?

A

the kidney

29
Q

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

A

The RAAS

30
Q

What to renal juxtaglomerular cells produce?

A

renin and angiotensin

31
Q

Where are renin and angiotensin produced?

A

by the renal juxtaglomerular cells

32
Q

What stimulates renin and angiotensin production?

A

sympathetic stimulation
decreased BP
decreases Na+ absorption

33
Q 
What do....
sympathetic stimulation
decreased BP
decreases Na+ absorption
....cause?
A

production of renin and angiotensin

34
Q

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

A

Renin

35
Q

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

A

angiotensinogen

36
Q

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

A

angiotensin I (AI)

37
Q

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

A

Angiotensin I

38
Q

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

A

Angiotensin Converting Enzyme (ACE)

39
Q

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

A

Angiotensin II (AII)

40
Q

What are ACE inhibitors and angiotensin II receptor blockers?

A

tx for HTN and HF

41
Q

What is the direct affect of angiotensin II?

A

causes vasoconstriction by binding to GPCRs

42
Q

What is the indirect affect of angiotensin II?

A

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

43
Q

What is aldosterone?

A

a steroid hormone produced by the adrenal cortex

44
Q

What does aldosterone do?

A

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

45
Q

What is ADH?

A

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

46
Q

What stimulates ADH release?

A 
hypovolemia
hypotension
high osmolarity
angiotensin II
SNS
47
Q

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

A

vasoconstriction

48
Q

What is the purpose of the RAAS system?

A

to increase BP and blood volume

49
Q

What is atrial natriuretic peptide (ANP)?

A

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

50
Q

What does natriuretic mean?

A

sodium excreting

51
Q

What does ANP bind to?

A

natriuretic peptide receptors, not GPCRs, to produce cGMP

52
Q

What are cGMP’s affects?

A

activates SERCA, stimulates Ca++ uptake

53
Q

ANP increases the _____ and secretion of ____ and ____.

A

glomerular filtration rate; Na, water

54
Q

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

A

vasodilator; aldosterone and renin

55
Q

What are the immediate effects of standing?

A
  1. R atrial pressure drops

2. venous pressure in the legs increases

56
Q

What is orthostatic hypertension?

A

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

57
Q

When is the effect of orthostatic hypertension more pronounced?

A

in warm weather bc of vasodilation in the skin

58
Q

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

A

sympathetic; parasympathetic; the central command mechanism

59
Q

What is the central command mechanism?

A

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

60
Q

Activity of skeletal muscles increases venous return,

which increases _____ via the Frank-Starling mechanism.

A

stroke volume

61
Q

Activity of skeletal muscles increases venous return,

which increases stroke volume via the _____ mechanism.

A

Frank-Starling

62
Q

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

A

vasoactive metabolites

CVPR Exam I (29 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions