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P1: Card System > 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)

eg. Paracrine and autocrine( cell produces substances that work on itself)
Vasodilalators eg inflammation, local metabolites such as Nitric oxide, Prostaglandins, Endothelin, K+, H+

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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
eg. Parasympathetic, sympathetic & sensory vasodilator nerves

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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

Beta 1-increase HR and SV

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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 & PGE1, 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
1 action potential per second

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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

Rostral ventrolateral medulla (RVLM) – this is controlled by other areas such as…

Caudal ventrolateral medulla (CVLM) & hypothalamus.
Provides central control of blood flow & blood pressure.

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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

Produces vascular tone allows vasodilatation/increased blood flow to occur, controls TPR.
→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.

A few sympathetic vasodilator nerves exist
eg. Sensory (nociceptive C fibres) vasodilator fibres

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20
Q

How does vasodilation occur?

A

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

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21
Q

What are the innervations of vasodilator nerves?

A

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

These release acetylcholine (Ach) which binds to muscarinic receptors on the smooth muscle and/or endothelium.

M3 receptors located on the vascular endothelium can coupled to the formation of nitric oxide (NO) causing vasodilation.

However, ACh also can also cause contraction through smooth muscle M2 and M3 receptors.

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22
Q

Where are parasympathetic vasodilator nerves found?

A

→salivary glands (release Ach and VIP)
→ pancreas and intestinal mucosa (release VIP)Both these tissues need high blood flow to maintain fluid secretion.
Ach/VIP act on endothelium to cause release of nitric oxide (NO) - vasodilatation

→ male genitalia (release NO)

23
Q

Where are sympathetic vasodilator nerves found?

A

→skin (sudomotor fibres) (release Ach and VIP)
→causing vasodilatation via NO associated routes.
Increased blood flow causes more sweat and also allows heat loss via skin.

24
Q

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

A

→The stimulation of 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- degranulation
→ 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- 453 a.a
3) undergoes proteolysis and becomes Angiotensin I(decapeptide) which goes to the lungs
4) Angiotensin converting enzyme converts it into Angiotensin II (increased sympathetic drive, thirst) octapeptide
5) Aldosterone is produced causes renal NaCl + H2O retention - raises blood volume

38
Q

What are the central effects of angiotensin II?

A

increased sympathetic drive; thirst so increases blood volume.
More sympathetic tone; raising BP and decrease hydrostatic pressure in the capillaries and reduce the amount of fluid squeezed out into the interstitial fluid

  1. vasoconstriction raises TPR
39
Q

What is the hypothalamus response stimulated by?

A

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

40
Q

Where is vasopressin or ADH released from?

A

→ Posterior of the pituitary gland

41
Q

What does vasopressin or ADH release cause?

A

→ Vasoconstriction and increases renal absorption of water

→ maintains blood pressure

42
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

43
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.

→Hypothalamus response stimulated by an increase in osmolarity ie dehydration or low blood volume.

→Vasopressin (ADH) released from the posterior of pituitary gland causes increased reabsorption of fluid by kidney and also causes vasoconstriction - both effects maintain blood pressure.

44
Q

What is ANP released by?

A

→ Specialised atrial myocytes

45
Q

how is ANP is secreted?

A

→ Secreted by increased filling pressures which stimulate stretch receptors

46
Q

Where does ANP act?

A

→ Acts at NP receptors on vascular smooth muscle cells
→Increases the cGMP pathway (like NO)
→ANP mediated dilation and increase in glomerular filtration

47
Q

What does ANP do?

A

→ Systemic vasodilation

→Opposes the action of RAAS, ADH and noradrenaline

48
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

49
Q

Describe the sympathetic vasoconstrictor system

A
  1. Nervous system information integrated by brain
  2. Main excitatory drive
  3. Thoracic (T1-L2) spinal cord. Intermediolateral cell column (IML). Contains pre-ganglionic sympathetic neurones
  4. Sympathetic preganglionic fibre
  5. sympathetic ganglia
  6. Sympathetic
    postganglionic fibre
  7. Adrenal medulla. Adrenaline partly under parasympathetic influence
50
Q

Where are varicosities found?

A

tunica adventia

51
Q

What types of receptors do cerebral arteries have?

A

M5muscarinic receptors that vasodilate in response to ACh.

52
Q

Parasympathetic innervations of the male genitalia

A

– release NO

Release of NO by parasympathetic nerves causes production of cGMP which leads to vasodilatation.

53
Q

How does viagra(sildenafil) work?

A

enhances this effect of NO by inhibiting the breakdown of cGMP by phosophodiesterase-5.

P1: Card System (16 decks)

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