Nervous & hormonal control of vascular tone Flashcards
What is intrinsic control
Regulate local blood flow to organs/tissues
Examples of intrinsic control
Vasoconstrictors e.g. myogenic response
Vasodilators e.g. inflammation
Nitric oxide, prostaglandis, endothelin, K+, H+
What is extrinsic control
Regulate TPR to control Blood pressure
Examples of extrinsic control
NERVES:
Vasoconstrictors - noradrenaline
Vasodilators - ACh, NO
HORMONES:
Vasoconstrictor - adrenaline, angiotensin II, Vasopressin
Vasodilator - Anti-natriuretic peptide (ANP)
The steps for stimulation of sympathetic vasoconstrictor nerves
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
How is the release of NA modulated
By Angiotensin II acting on AT1 receptor, increasing NA release
What metabolites prevent vasoconstriction
K+, adenosine, histamine and serotonin
NA can negatively feedback itself via α2 receptors to limit its own release
Sympathetic vasoconstrictor nerves
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
Main roles of sympathetic vasoconstrictor nerves
Distinct RVLM neurones-sympathetic pathways innervate different tissues
Control venous blood volume
Pre-capillary vasoconstriction
Contract resistance arterioles
Why controlling venous blood volume is important
Venoconstriction leads to decreased venous blood volume increasing venous return. This increases SV via Starling’s law
Why is pre-capillary vasoconstriction important
Leads to downstream capillary pressure drop so increased absorption of interstitial fluid into blood plasma to maintain blood volume
Why is contract resistance arterioles important
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
Vasodilator nerves
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
Effects of ACh on different receptors
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
Sympathetic vasodilator nerves
Skin (sudomotors) - release ACh and VIP –> vasodilation via NO associated routes
Increase blood flow = more sweat and lose heat via skin
Parasympathetic vasodilator nerves
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
Hormones causing vasoconstriction
Adrenaline
Angiotensin II
Vasopressin (ADH)
Hormones causing vasodilators
Atrial netrieutic peptide (ANP)
Other hormones affecting vasculature
Insulin, oestrogen, relaxin
Adrenaline
Released from adrenal medulla - via action of ACh on nicotinic receptors
What are the main roles of Adrenaline
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
Adrenaline vs Noradrenaline on resistance vessels
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
Vasopressin (ADH)
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
Atrial natriuretic peptide (ANP)
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)
System vasodilation
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
