Nervous & hormonal control of vascular tone

Question 1

What is intrinsic control

Answer 1

Regulate local blood flow to organs/tissues

Question 2

Examples of intrinsic control

Answer 2

Vasoconstrictors e.g. myogenic response
Vasodilators e.g. inflammation
Nitric oxide, prostaglandis, endothelin, K+, H+

Question 3

What is extrinsic control

Answer 3

Regulate TPR to control Blood pressure

Question 4

Examples of extrinsic control

Answer 4

NERVES:
Vasoconstrictors - noradrenaline
Vasodilators - ACh, NO

HORMONES:
Vasoconstrictor - adrenaline, angiotensin II, Vasopressin
Vasodilator - Anti-natriuretic peptide (ANP)

Question 5

The steps for stimulation of sympathetic vasoconstrictor nerves

Answer 5

1) An action potential moves down the axon and arrive at a varicosity
2) Depolarisation at the varicosity activating voltage gated Ca2+ channels
3) Ingress of calcium causes release of neurotransmitters - mainly noradrenaline
4) NA diffuses to the vascular smooth muscle cells where it binds mainly α1 – contraction; some α2 – contraction and β2 – relaxation. Modulation of responses in both constriction and dilatation.
5) The noradrenaline is then taken up again and recycled or broken down

Question 6

How is the release of NA modulated

Answer 6

By Angiotensin II acting on AT1 receptor, increasing NA release

Question 7

What metabolites prevent vasoconstriction

Answer 7

K+, adenosine, histamine and serotonin

NA can negatively feedback itself via α2 receptors to limit its own release

Question 8

Sympathetic vasoconstrictor nerves

Answer 8

Controlled by brainstem - RVLM - provides central control of blood flow and BP

Innervate most arterioles and veins - o NA activates α1 adrenoceptors on vascular smooth muscle cells causing vasoconstriction

Question 9

Main roles of sympathetic vasoconstrictor nerves

Answer 9

Distinct RVLM neurones-sympathetic pathways innervate different tissues
Control venous blood volume
Pre-capillary vasoconstriction
Contract resistance arterioles

Question 10

Why controlling venous blood volume is important

Answer 10

Venoconstriction leads to decreased venous blood volume increasing venous return. This increases SV via Starling’s law

Question 11

Why is pre-capillary vasoconstriction important

Answer 11

Leads to downstream capillary pressure drop so increased absorption of interstitial fluid into blood plasma to maintain blood volume

Question 12

Why is contract resistance arterioles important

Answer 12

Produces vascular tone allows vasodilation/increased blood flow to occur, controls TPR
Maintains arterial blood pressure and blood flow to brain myocardium and kidney etc

Question 13

Vasodilator nerves

Answer 13

Vasodilation usually occurs as vascular tone produced by sympathetic vasoconstrictor nerves is inhibited
Specific vasodilator nerves are mainly parasympathetic
Some blood vessels are innervated by parasympathetic cholinergic fibres - release ACh which binds to muscarinic receptors on smooth muscle/endothelium

Question 14

Effects of ACh on different receptors

Answer 14

M3 receptors - vascular endothelium can couple to formation of nitric oxide (NO) causing vasodilation
Cause contraction through smooth muscle M2 and M3 receptors
Cerebral arteries appear to have M5 muscarinic receptors that produce vasodilation in response to ACh

Question 15

Sympathetic vasodilator nerves

Answer 15

Skin (sudomotors) - release ACh and VIP –> vasodilation via NO associated routes
Increase blood flow = more sweat and lose heat via skin

Question 16

Parasympathetic vasodilator nerves

Answer 16

Salivary glands - release ACh and VIP
Pancrease & intestinal mucosa - release VIP
ACh/VIP act on endothelium to cause release of NO - vasodilation
Male genitalia - release NO by parasympathetic nerves producing cGMP –> vasodilation

Question 17

Hormones causing vasoconstriction

Answer 17

Adrenaline
Angiotensin II
Vasopressin (ADH)

Question 18

Hormones causing vasodilators

Answer 18

Atrial netrieutic peptide (ANP)

Question 19

Other hormones affecting vasculature

Answer 19

Insulin, oestrogen, relaxin

Question 20

Adrenaline

Answer 20

Released from adrenal medulla - via action of ACh on nicotinic receptors

Question 21

What are the main roles of Adrenaline

Answer 21

Metabolic and CVS effects:
Glucose mobilisation (skeletal muscle glycogenolysis, fat lipolysis)
Stimulation of heart rate and contractility during normal excercise
Vasodilation of coronary and skeletal muscle arteries

Question 22

Adrenaline vs Noradrenaline on resistance vessels

Answer 22

In most tissue vasoconstriction due to α1 adrenoceptors
Skeletal muscle and coronary arteries have more α2 than α1 adrenoceptors
Adrenaline higher affinity for β over α, mainly acts at β2 to dilate vessels
Noradrenaline higher affinity for α, mainly acts at α1 receptors to constrict vessels

Question 23

Vasopressin (ADH)

Answer 23

Stretch receptors in the left atrium send continuous signals causes to NTS
The NTS sense out inhibitory nerves to the CVLM
CVLM signals stimulate pituitary to release vasopressin so stretching of the heart inhibits this
Dehydration of haemorrhage NTS inhibition is switched off and CVLM stimulates vasopressin.
NTS is the thermostat that sets the level at which the CVLM is inhibited
Hypothalamus response stimulated by an increase in osmolarity e.g. dehydration of low blood volume
Vasopressin (ADH) released from the posterior of pituitary gland causes increased reabsorption of fluid by kidney and causes vasoconstriction – both effects maintain blood pressure

Question 24

Atrial natriuretic peptide (ANP)

Answer 24

ANP released by specialised atrial myocytes
Secreted by increased filling pressures which stimulate stretch receptors
Act at ANP receptors on vascular smooth muscle cells increasing cGMP pathway (like nitric oxide)

Question 25

System vasodilation

Answer 25

Opposes action of noradrenaline, RAAS, ADH
Dilatation of renal afferent arteriole increases GFR
Na+ and H2O excretion by the kidney are increased and blood volume goes down decreasing release and actions of aldosterone, renin and ADH