nervous and hormonal control of vascular tone Flashcards

1
Q

What is involved in intrinsic control of blood vessels

A
  • myogenic response
    -paracrine & autocrine
  • physical factors -temperature & shear pressure
    -regulates blood flow to organs and tissues
    -vasodilators-inflammation , local metabolites ( nitric oxide, prostaglandin, endothelin, potassium and hydrogen ions )
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2
Q

What is involved in extrinsic control of blood vessels

A
  • parasympathetic , sympathetic and sensory vasodilator nerves
    -sympathetic vasoconstrictor nerves
    -brain Function selectivity alters blood flow to organs according to need

In the nerves
Vasoconstrictor- noradrenaline
Vasodilators - Ach, nitric oxide

In hormones
Vasoconstrictor- adrenaline, angiotensin II
Vasodilator- atrial natriuretic peptide (ANP)

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3
Q

Steps for constriction in sympathetic vasoconstrictor nerves

A
  • action potential moves down axon and arrive at varicosity
  • depolarisation at the varicosity activating voltage gated calcium channels
  • entrance of calcium causes release neurotransmitters- mainly noradrenaline
  • noradrenaline diffuses to vascular smooth muscle cells binds to mainly alpha one , some alpha two and beta two

-noradrenaline is taken up again and recycled or broken down

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4
Q

What is the release of noradrenaline modulated by

A

Angiotensin II acting on AT1 receptor

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5
Q

what is varicosity

A

veins that are bulging and swollen

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6
Q

what happens when noradrenaline is released in the varicosity detail

A

noradrenaline is released which causes vasodilation via alpha 1 receptors

alpha 2 receptors provide negative feedback so that the noradrenaline doesnt continuously lead to constriction

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7
Q

what is the rostal ventrolateral medulla controlled by and its role

A

caudal ventrolateral medulla and hypothalamus and provides central control of blood flow and blood pressure

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8
Q

how is the sympathetic nerve activity described as

A

tonic, 1 action potential per second

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9
Q

in sympathetic vasoconstrictor nerves what does noradrenaline activate and cause

A

activates alpha 1 adrenoreceptors on vascular smooth muscle cells causing vasoconstriction

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10
Q

main roles of sympathetic vasoconstrictor nerves

A

-distinct sympathetic pathways ( switching on vasoconstriction in some vessels )

-control resistance arterioles (produces vascular tone allows vasodilation or vasoconstriction , maintains arterial blood pressure and blood flow to brain myocardium

-precapillary vasoconstriction ( downstream capillary pressure drop so increased absorption of interstitial fluid into blood plasma to maintain blood volume)

-control venous blood volume ( venoconstriction leads to decreased venous blood volume increasing venous return , increases stroke volume via starlings law

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11
Q

when does vasodilation usually occur

A

when vascular tone produced by sympathetic vasoconstrictor nerves is inhibited

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12
Q

are specific vasodilator nerves sympathetic or parasympathetic

A

parasympathetic

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13
Q

in vasodilator nerves what are blood vessels innervated by

A

parasympathetic cholingeric fibres , they release acetylcholine which binds to muscarinic receptors on the smooth muscle or endothelium

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14
Q

example of parasympathetic vasodilators

A

-salivary glands- release ach and VIP

-pancreas and intestinal mucosa - release VIP , both need high blood flow to maintain fluid secretion.

male gentalia - erectile tissue , release nitric oxide by sympathetic nerves causes production of cGMP which leads to vasodilation

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15
Q

examples of sympathetic vasodilators

A

-skin -sudomotor fibres, release Ach , VIP causing vasodilation via nitric oxide associated with sweating

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16
Q

what does sympathetic activity vasoconstriction

A

-reduces blood flow , limit sweat production and limit cooling

17
Q

what is the lewis triple response

A

inflammation
-redness caused by capillary vasodilation

-flare-redness in surrounding area due to arteriolar dilation mediated by axon reflex

-wheal- exudation of extracellular fluid from capillaries and venules

18
Q

hormones involved in vasoconstriction

A

-adrenaline
-angiotensin II
-vasopressin - ADH

19
Q

hormone involved in vasodilation

A

-ANP - atrial natriuretic peptide

20
Q

where is adrenaline released from and when

A

adrenal medulla via action of acetylcholine on nicotinic receptors
during
-exercise
-flight-fight-fear response
-hypotension
-hypoglycaemia

21
Q

main role of adrenaline (epinephrine)

A

-glucose mobilisation

-stimulation of heart rate & contractility during normal exercise

-vasodilation of coronary and skeletal muscle arteries

22
Q

action of noradrenaline on resistance vessels

A

-activate alpha 1 Gq
-leads to phospholipase c
-leads to PIP2 converting to IP3 and DAG
-calcium ions are released
-smooth msucle contraction

23
Q

action of adrenaline on resistance vessels

A

-activates beta 1 and beta 2 Gs
-leads to adenylate cyclase
-converts ATP to cAMP
-leads to beta 1 heart contraction
-beta 2 smooth muscle relaxation vasodilation

24
Q

what does adrenaline have a higher affinity for

A

higher affinity for beta over alpha , mainly acts at beta 2 to dilate vessels

25
Q

what does noradrenaline have a higher affinity for

A

higher affinity for alpha, mainly acts at alpha 1 to constrict vessels

26
Q

role of beta 1 on heart

A

increases rate and force of contraction

27
Q

role of alpha 2

A

inhibits adenylate cyclase , reduces calcium ions , inhibits release of noradrenaline from varicosity

28
Q

steps in renin angiotensin aldosterone system (RAAS)

A

-low sodium load , detected at macula densa
-decreased pressure at juxtagomerular cells
-leads to renal sympathetic activity
-renin released
-conversion of angiotensinogen to angiotensin I
-occurs in lung vascular endothelium
-angiotensin 2 is produced from angiotensin 1
-aldosterone released
-central effects eg thirst
-vasoconstriction raises TPR
-release of vasopressin (ADH)
-Aldosterone leads to renal sodium chloride and water retention -raised blood volume

29
Q

how are vasopressin stimulated to be released

A

-dehydration/ haemorrhage NTS inhibition is switched off and CVLM stimulates vasopressin

30
Q

when there is an increase in osmolarity what does this lead to

A

-vasopressin synthesised in hypothalamus
-released from vesicles in posterior of pituitary gland
-leads to insertion of water aquaporin channels into apical membrane of renal collecting tubule
-collecting duct epithelial cells allowing water to move out of the nephron and back into the blood stream
-reabsorption of fluid by kidney and vasoconstriction both maintain blood pressure

31
Q

what is ANP released and secreted by

A

-released by atrial myocytes

-secreted by increased filling pressures which stimulate stretch receptors

32
Q

where does ANP act

A

acts at ANP receptors on vascular smooth muscle cells increasing cGMP pathway (like nitric oxide)

33
Q

what does systemic vasodilation oppose

A

action of noradrenaline, RAAS, ADH