055 Nervous, Local, Humorol Control of Vascular Resistance Flashcards

1
Q

Why does radius have such a large impact on resistance?

A

Resistance is directly proportional to 1/r^4. So a small increase in radius will cause a huge drop in resistance.

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

Between which vessels is the most significant pressure drop? and why?

A

Arterioles have a huge drop in blood flow. There is also increase in resistance due to sudden decrease in radius. There is significant blood pressure drop.

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

What is the relative wall/lumen ratio of resistance vessels and why?

A

1:1 due to the thick smooth muscle layer that has vascular tone caused by the background sympathetic drive to its a1 receptors.

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

Explain the mechanism of sympathetic activation causing smooth muscle contraction.

A

noradrenaline stimulates a1 adrenoreceptors, causing smooth muscle contraction.

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

In which vascular beds is parasympathetic innervation important?

A

Erectile tissue and the cerebral system

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

How is angiotensin II formed from the precursor form? What effect does angiotensin II have?

A

Angiotensin converting enzyme is found on endothelial cells, converting angiotensin I (found in the blood) to angiotensin II. It is activated by the release of rennin from the juxtagloremular apparatus.

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

Explain the mechanism of adrenaline on different types of adrenoreceptors and the consequent effects.

A

a1 receptors - smooth muscle vasoconstriction in all other vascular beds.
b2 receptors - cAMP is increased causing vasodilation of arterioles in skeletal muscle and the heart.

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

What is the difference between functional and reactive hyperaemia?

A

Functional hyperaemia occurs when there is an increased metabolic demand for oxygen e.g. exercise, causing an vasodilation to increase blood flow. Reactive hyperaemia occurs after an occlusion to an arterial. The blood flow following the interuption of arterial supply is above the level that occured before the occlusion.

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

What is the difference between autoregulation and hyperaemia?

A

auto regulation occurs when there is increased perfusion pressure but constant metabolic demand. Hyperaemia occurs when there is changing metabolic demand and a need for a changing perfusion pressure.

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

What is endothelin and what can stimulate its release?

A

This is a vasoconstrictor that released by the endothelium. Humoral factors such as angiotensin, vasopressin, thrombin can induce endothelin.

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

In which 2 locations are natriuretic peptides produced? What are they?

A

BNF (Brain natriuretic factor) is produced in the ventricles when stimulated by stretch or sympathetic activity e.g. increased preload. They will cause vasodilation. ANF (Atrial natriuretic factor) is produced in the atrium when stimulated by stretch or sympathetic activity.

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

Where is vasopressin made and where is it released?

A

Made in the hypothalamus and released in the pituitary glands

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

What effect does vasopressin have on the body?

A

Vasoconstrictor - activates V1 receptors.

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

What are the 3 endothelium-derived factors that cause smooth muscle relaxation?

A

EDHF, NO, Prostacyclin

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

How does exercise cause vasodilation?

A

When you exercise, the increase in blood flow will raise shear stress. This activates the NOS pathway, producing NO and activating sGC, cCMP etc. Vasodilation then occurs.

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

What are the neuronal factors that change vascular resistance?

A

Sympathetic nervous system and parasympathetic nervous system.

17
Q

What is the pathway for NO in response to shear stress, hypoxia, or autocoids?

A

Shear stress, hypoxia, or autocoids stimulate NOS which activates NO. NO activates sGC (Guanyl cyclase), which then phosphorylates cCMP causing relaxation.

18
Q

What is the pathway for EDHF in response to hear stress, hypoxia, or autocoids?

A

EDHF -> increasing hyperpolarization -> prolonged relaxation

19
Q

What does EDHF stand for and in which vascular bed is it most significant?

A

Endothelial derived hyper polarizing factors, most significant in arterioles

20
Q

What is are source of Ca2+ transport in smooth muscle fibres?

A

Voltage gated Ca2+ ion channels that is stimulated by protein Gq (which is activated by adrenaline). Non-selective cation channels are also stimulated to open when muscle is stretched.

21
Q

What are 4 humoral agents released to control vascular resistance?

A

Adrenaline - dilating skeletal and heart vessels but constricting smooth muscle in arterioles.
Vasopressin - vasoconstriction in smooth muscles but vasodilation in the heart and the brain.
Angiotensin II - vasoconstrictor by AT1 receptors and increased sympathetic drive
Natr

22
Q

What are functional and reactive hyperaemia mediated by?

A

Hypoxia or metabolites released from tissue surrounding blood vessels e.g. adenosine, H+, CO2, K+ that act directly on smooth muscle.

23
Q

What is autoregulation of vascular beds?

A

When smooth muscle changes blood flow during a change in perfusion pressure but a constant metabolic demand. This occurs in the skeletal blood, mycardium, and brain. It prevents any unnecessary increases in blood flow.

24
Q

How do platelets affect vascular beds?

A

Increase in platelet aggregation causes endothelium dependant vasodilation. They release autocoids, ADP, and other vasodilators. This is a self protective mechanism that prevents the thrombin formation.

25
Q

What is are source of Ca2+ transport in smooth muscle fibres?

A

Voltage gated Ca2+ ion channels that is stimulated by protein Gq (which is activated by adrenaline). Non-selective cation channels are also stimulated to open when muscle is stretched.

26
Q

Where is vasopressin released?

A

Posterior pituitary gland

27
Q

How is the vasopressin stimulated?

A

Increased osmolarity or decreased baroreceptor drive causes hypothalamus to signal to the pituitary gland.

28
Q

What are 4 humoral agents released to control vascular resistance?

A

Adrenaline - dilating skeletal and heart vessels but constricting smooth muscle in arterioles.
Vasopressin - vasoconstriction in smooth muscles but vasodilation in the heart and the brain.
Angiotensin II - vasoconstrictor by AT1 receptors and increased sympathetic drive
Natriuretic peptide hormones - vasodilation in response to stretch receptors or sympathetic activation

29
Q

What is the pathway of the endothelium vasodilation by prostaglandins in response to shear stress, hypoxia, or autocoids?

A

Shear stress, hypoxia, or autocoids stimulate COX (cyclic oxidase) which then activate the PG prostaglandin. This activates a G-protein Gs in the smooth muscle, which causes AC (adenocyclase) to catalyze and form cAMP, causing relaxation.

30
Q

What is the pathway for NO in response to shear stress, hypoxia, or autocoids?

A

Shear stress, hypoxia, or autocoids stimulate NOS which activates NO. NO activates sGC (Guanyl cyclase), which then catalyzes GTP to cCMP, causing relaxation.