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

• < 60 mmHg see no stimulation of baroreceptors

• 60 - 160 mmHg see maximum stimulation

• see maximum at normal pressures [I = impulses]

• the baroreceptors respond much more to a rapidly changing pressure than to a stationary pressure

• they adapt in 1 — 2 days to whatever pressure they are exposed to; have no long term effect in BP regulation

baroreceptor reflex

• stimulated baroreceptors inhibit vasoconstrictor centre of medulla —>

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 < 80 mm Hg

3) ATRIAL & PULMONARY ARTERY REFLEXES

Anatomy

• Both the atria & pulmonary arteries have stretch receptors in their walls—low pressure receptors

• pulmonary artery receptors are similar to baroreceptors in operation, atrial receptors operate as follows:

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 < 50 mmHg — ‘last ditch stand’

• Cushing reaction: increased Intracranial pressure —> 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

• at least 20 minutes are required before this system can become fully active

• it has a relatively long duration of action