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Physiology 1 : cardiovascular > Nervous and hormonal control of vascular tone > Flashcards

Nervous and hormonal control of vascular tone Flashcards

1
Q

What is intrinsic control?

A

→ Regulates local blood flow to organs/ tissues

→ Important - regional hyperaemia (increase in blood flow)

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2
Q

What is extrinsic control?

A

→ Regulates TPR to control blood pressure

→ Brain function selectivity alters blood flow to organs according to need

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3
Q

What are vasoconstrictor hormones?

A

→ Adrenaline, angiotensin II, vasopressin

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4
Q

What is a vasodilator hormone?

A

→ Atrial Natriuretic Peptide

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5
Q

What is the most widespread and important form of extrinsic control?

A

→Sympathetic vasoconstriction

→ Nervous system information integrated by the brain

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6
Q

How does sympathetic innervation of the arterioles leads to release of NA?

A

1) Action potential moves down the axon and arrives at a varicosity
2) Depolarization at the varicosity activates voltage gates Ca2+ channels
3) Ingress of Ca2+ causes the release of neurotransmitters - mainly NA
4) NA diffuses into the vascular smooth muscle cells

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7
Q

What are the three receptors NA binds to and what are the effects?

A

→ alpha 1 - contraction
→ alpha 2 - contraction
→ beta 2 - relaxation

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8
Q

How can the release of NA be modulated?

A

→ by Angiotensin II acting on AT 1 receptor which increases NA release
→metabolites prevent vasoconstriction and maintain blood flow
→K+, adenosine, histamine & serotonin feedback and inhibit NA release
→ NA can also negatively feed back itself via a2 receptors to limit its own release.

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9
Q

what does lots of modulation occurring at the NT level produce?

A

→ Produces vasoconstriction + vasodilation as required

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10
Q

What are sympathetic vasoconstrictor nerves controlled by?

A

→ controlled by the brain stem (provides control of blood flow/ blood pressure)

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11
Q

What do sympathetic vasoconstrictor nerves innervate?

A

→innervates most of the arterioles and veins of the body

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12
Q

What kind of activity do sympathetic nerves have?

A

→sympathetic nerve activity is tonic

→ tonic sympathetic activity sets vascular tone

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13
Q

What is an important principle in pharmacological treatment of CVS diseases with regards to sympathetic activity?

A

→a decrease in sympathetic activity producing vasodilation is an important principle in pharmacological treatment of cardiovascular disease

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14
Q

How do sympathetic vasoconstrictor nerves contract resistance arterioles?

A

Produce vascular tone which allows vasodilation/increased blood flow to occur which controls TPR

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15
Q

What do DISTINCT RVLM NEURONES do?

A

(sympathetic pathways innervate different tissues)

we can switch vasoconstriction on in some vessels and off in others

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16
Q

What does pre-capillary vasoconstriction do?

A

→this leads to a downstream capillary pressure drop

→ increased absorption of interstitial fluid into the blood plasma to maintain blood volume

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17
Q

How do sympathetic vasoconstrictor nerves control TPR?

A

→it maintains arterial blood pressure and blood flow to the brain/myocardium area (since Pa = CO x TPR)

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18
Q

What does venoconstriction lead to?

A

→ venoconstriction leads to a decreased venous blood volume
→ increasing the venous return
→ increases the stroke volume via Starling’s Law

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19
Q

What types of tissues contain vasodilator nerves and what is their function?

A

→ A few specialised tissues contain vasodilator nerves, as well as vasoconstrictor nerves.
→ they have a specific function controlling a specific vascular bed rather than global functions.

20
Q

How does vasodilation occur?

A

Vasodilation occurs as the vascular tone produced by sympathetic vasoconstrictor nerves is inhibited.

21
Q

What are the innervations of vasodilator nerves?

A

There are mainly parasympathetic vasodilator nerves, and a few sympathetic vasodilator nerves

22
Q

Where are parasympathetic vasodilator nerves found?

A

→salivary glands (release Ach and VIP)
→ pancreas and intestinal mucosa (release VIP)
→ male genitalia (release NO)

23
Q

Where are sympathetic vasodilator nerves found?

A

→skin (sudomotor fibres) (release Ach and VIP)

24
Q

Describe the effect of stimulation of sensory (nociceptive C fibres) vasodilator fibres

A

→The stimulationof sensory axon reflex (C-fibres) occurs by trauma, infection, etc.

→They release a substance called substance P or calcitonin gene-related peptide (CGRP).

→This acts on mast cells to release histamine.
→ It also acts on the endothelium and vascular smooth muscle.

→Both the histamine and CGRP produce vasodilation, seen as the ‘flare’ in the skin.

25
Q

What is the Lewis triple response?

A

→ Local redness
→ Wheal
→ Flare

26
Q

What are 3 vasoconstrictor hormones?

A

→ Adrenaline
→Angiotensin II
→ Vasopressin (ADH)

27
Q

What are 3 hormones that affect the circulation?

A

→ estrogen, insulin, relaxin

28
Q

Where is adrenaline released from?

A

→ Adrenal medulla via the action of AcH on nicotinic receptors

29
Q

When is adrenaline released?

A

→ Exercise
→ fight or flight
→ Hypotension
→ Hypoglycaemia

30
Q

What are the main roles of adrenaline?

A

→ Glucose mobilization (skeletal muscle, glycogenolysis, fat lipolysis)
→ Stimulation of the heart rate and contractility during normal exercise
→ Vasodilation of coronary and skeletal muscle arteries

31
Q

Why is there vasoconstriction in most tissue?

A

→ due to alpha 1 adrenoceptors

32
Q

What receptors do skeletal muscles and coronary arteries have more of?

A

→ more beta 2 than alpha 1 adrenoceptors

33
Q

What receptor does adrenaline have a higher affinity for?

A

→ Higher affinity for beta over alpha

34
Q

What receptor does noradrenaline have a higher affinity for?

A

→ Higher affinity for alpha

35
Q

Describe the effects of iv adrenaline on the heart

A

→ the heart rate increases.
→The cardiac output also increases
→ total peripheral resistance decreases (due to its effects on the β2 receptors)
→ not much of an effect on blood pressure.

36
Q

Describe the effects of iv noradrenaline on the heart

A

→ big increase in TPR (due to vasoconstriction at the α1 receptors)
→ causes an increase in blood pressure.
→ increased BP stimulates the baroreceptors’ reflex to decrease heart rate.

37
Q

How does the RAAS system work?

A

1) Renin is produced by the kidney, stimulated by low renal blood flow
2) Angiotensinogen is the precursor produced in the liver
3) undergoes proteolysis and becomes Angiotensin I which goes to the lungs
4) Angiotensin converting enzyme converts it into Angiotensin II (increased sympathetic drive, thirst)
5) Aldosterone is produced causes renal NaCl + H2O retention - raises blood volume

38
Q

What is the hypothalamus response stimulated by?

A

→ An increase in osmolarity (dehydration or low blood volume)

39
Q

Where is vasopressin or ADH released from?

A

→ Posterior of the pituitary gland

40
Q

What does vasopressin or ADH release cause?

A

→ Vasoconstriction and increases renal absorption of water

→ maintains blood pressure

41
Q

how does vasopressin respond to lowered BP?

A

→Stretch receptors in the left atrium send continuous signals, causing firing in the NTS (nucleus tractus solitarius).

→This sends out inhibitory signals to the CVLM.

→The CVLM (caudal ventrolateral medulla) stimulates the pituitary to release ADH

→ stretching of the heart inhibits release of ADH

42
Q

What happens to the NTs during dehydration or haemorrhage?

A

→NTS’s inhibition is switched off and the CVLM stimulates vasopressin production.
→ The NTS is like the thermostat that sets the level at which the CVLM is inhibited.

43
Q

What is ANP released by?

A

→ Specialised atrial myocytes

44
Q

how is ANP is secreted?

A

→ Secreted by increased filling pressures which stimulate stretch receptors

45
Q

Where does ANP act?

A

→ Acts at NP receptors on vascular smooth muscle cells

→Increases the cGMP pathway (like NO)

46
Q

What does ANP do?

A

→ Systemic vasodilation

→Opposes the action of RAAS, ADH and noradrenaline

47
Q

What does the dilation of the renal afferent arteriole do?

A

→ Increases GFR
→ Na+ and H2O excretion by the kidney are increased
→ blood volume goes down decreasing the release and/or actions of aldosterone, renin + ADH

Physiology 1 : cardiovascular (18 decks)

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