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
2
Q
What does myogenic response counteract?
A
increased pressure
3
Q
The myogenic response can be overcome by ____.
A
vasoactive metabolites
4
Q
Give an example of when the myogenic response might kick in.
A
when you quickly stand up
5
Q
What channels cause the myogenic response?
A
stretch-activated ion channels of the Trp family
6
Q
Stretch-activated ion channels of the Trp family cause what?
A
the myogenic response
7
Q
What produces NO?
A
vascular endothelium via nitric oxide synthase
8
Q
What does NO do?
A
causes vasodilation
9
Q
Basal NO release helps to set the _____.
A
resting vascular tone
10
Q
A decrease in NO is one factor associated with risk of _____.
A
atherosclerosis
11
Q
What enzyme is sensitive to cigarette smoke, increasing risk of CVD?
A
nitric oxide synthase
12
Q
Nitric oxide synthase (NOS) produces NO from ____.
A
L-arginine and O2
13
Q
What does NO activate?
A
guanylyl cyclase, to produce cGMP
14
Q
What in the blood stimulates production of NO?
A
humoral agents, like bradykinin and ACh
15
Q
Humoral agents cause _____, which activates nitric oxide synthase (NOS).
A
an increase in intracellular Ca++
16
Q
- NO activates guanylyl cyclase to produce cGMP
- cGMP activates ____
- PKG reduces intracellular Ca++ via activation of SERCA and inhibition of L-type Ca++ channels
- Decreased Ca++ causes vasodilation via reduced MLCK activity
A
PKG
17
Q
- NO activates guanylyl cyclase to produce cGMP
- cGMP activates PKG
- PKG _____ via activation of SERCA and inhibition of L-type Ca++ channels
- Decreased Ca++ causes vasodilation via reduced MLCK activity
A
- NO activates guanylyl cyclase to produce cGMP
- cGMP activates ____
- PKG reduces intracellular Ca++ via activation of SERCA and inhibition of L-type Ca++ channels
- Decreased Ca++ causes vasodilation via reduced MLCK activity
18
Q
- NO activates guanylyl cyclase to produce cGMP
- cGMP activates PKG
- PKG reduces intracellular Ca++ via activation of ____ and inhibition of _____
- Decreased Ca++ causes vasodilation via reduced MLCK activity
A
SERCA; L-type Ca++ channels
19
Q
- NO activates guanylyl cyclase to produce cGMP
- cGMP activates PKG
- PKG reduces intracellular Ca++ via activation of SERCA and inhibition of L-type Ca++ channels
- Decreased Ca++ causes _____ via reduced MLCK activity
A
vasodilation
20
Q
- NO activates guanylyl cyclase to produce cGMP
- cGMP activates PKG
- PKG reduces intracellular Ca++ via activation of SERCA and inhibition of L-type Ca++ channels
- Decreased Ca++ causes vasodilation via _____
A
reduced MLCK activity
21
Q
- NO activates guanylyl cyclase to produce cGMP
- cGMP activates PKG
- PKG reduces intracellular Ca++ via activation of SERCA and inhibition of L-type Ca++ channels
- Decreased Ca++ causes vasodilation via reduced MLCK activity
A
NO action in vascular smooth muscle cells (VSMCs)
22
Q
Where is endothelin produced?
A
by the vascular endothelium
23
Q
What is endothelin?
A
a peptide that causes vasoconstriction
24
Q
What inhibits endothelin?
A
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
