Wednesday, October 7, 2009

Neurohumoral mechanism

Neurohumoral mechanism maintaining normal cardiac output and blood pressure



Acute haemorrhage —>

1) Rapidly acting pressure control mechanisms; to return blood pressure to physiological levels. All are nervous mechanisms:
i) Baroreceptor
ii) Chemoreceptor
iii) CNS ischaemic response

2) Long term mechanisms for arterial pressure regulation; to return blood volume to normal levels. Essentially involves kidney control via several hormonal mechanisms:
i) Renin — Angiotensin
ii) Aldosterone



SHORT TERM REGULATION OF MEAN ARTERIAL BLOOD PRESSURE

RAPIDLY ACTING NERVOUS MECHANISMS


1) BARORECEPTOR REFLEXES

Anatomy
• Baroreceptors are especially abundant in the:
a) carotid sinuses [located in wall of ICA just above carotid bifurcation]
b) walls of the aortic arch
• Impulses are transmitted from:
a) carotid sinus via the glossopharangeal nerve (CN-IX) to the medulla
b) aortic arch via the vagal nerve (CN-X) to the medulla


response of baroreceptors to pressure



• < i =" impulses]">
i) vasodilation of peripheral vasculature
ii) decreased HR & contractility
—> reduced BP
[low BP has an opposite effect]
• baroreceptors play a major role in maintaining BP during postural changes



2) CHEMORECEPTOR REFLEXES

Anatomy
• Chemoreceptors are located in the:
a) carotid bodies [located in the carotid bifurcation]
b) aortic bodies in walls of the aortic arch
• Impulses are transmitted via the vagus [along with nerve fibres from baroreceptors] into the vasomotor centre
• Each body has its own blood supply —> each body is in close contact with arterial blood

chemoreceptor reflex
• 1° reduced arterial BP —> reduced O2; increased CO2 & H+ —> stimulate chemoreceptors —> excite vasomotor centre —> increase BP
[& increased resp stim]
• 1°reduced O2; increased CO2 & H+ —> stimulate chemoreceptors —> excite vasomotor centre —> increase BP
• Only works strongly with BP < style="font-weight:bold;">atrial reflexes
• stretched atria —>
1) slight reflex vasodilation of peripheral arterioles —>
i) reduced peripheral resistance —> reduced BP back down to normal
ii) increased blood flow into capillaries —> increased capillary pressure —> third space shifting —> reduced blood volume
2) reflex dilatation of afferent arterioles of kidney —> increased urine production
3) stimulate hypothalamus —> decreased ADH —> reduced resorption of H2O in kidney —> increased urine secretion
4) increased HR [Bainbridge reflex] —> offload fluid from heart


4) CNS ISCHEMIC RESPONSE

• reduced blood flow to vasomotor centre in brain stem —> ischaemia of medulla —> increased local[CO2] —> excite vasomotor centre —> increased BP
• has a tremendous magnitude in increasing BP: is one of the most powerful activators of the sympathetic vasoconstrictor system
• Only becomes active at arterial BP <> compression of arteries in brain —> CNS ischaemic response —> increased BP


note that in all the above reflexes, the increased sympathetic output not only stimulates the arteries & arterioles but also constricts the veins —> increased mean systemic pressure —> increased cardiac output —> increased BP



RAPIDLY ACTING HORMONAL MECHANISMS

1) NORADRENALIN—ADRENALIN VASOCONSTRICTOR MECHANISM

• Sympathetic stimulation —> stimulate adrenal medulla —> release of Ad & NAd —> excite heart; vasoconstrict most blood vessels
• May act on metarterioles which are not innervated


2) VASOPRESSIN VASOCONSTRICTOR MECHANISM

• Reduced BP —> hypothalamus secretes vasopressin via post pituitary —> direct vasoconstriction —> increased peripheral resistance/MSFP —> increased BP
• Very potent; plays an important role in correcting BP when is acutely dangerously low —> important short term role
• Important long term role as ADH (same substance)


3) RENIN—ANGIOTENSIN VASOCONSTRICTOR MECHANISM
Decreased-BP -- RENIN


• at least 20 minutes are required before this system can become fully active
• it has a relatively long duration of action


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