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
