The various mechanisms that maintain a near-constant blood pressure in the body can be categorized into short-term mechanisms (baroreceptor reflexes), intermediate-term mechanisms (stress-relaxation and capillary fluid shift mechanism) and long-term mechanisms (pressure diuresis/natriuresis and Tenin-angiotensin mechanism).
Baroreceptor reflex prevents erratic fluctuations in blood pressures. Whenever the blood pressure changes rapidly, the baroreceptor reflex quickly brings about a negative feedback, correcting the initial change in blood pressure.
In the absence of the reflex, the blood pressure would fluctuate wildly during postural changes, emotional changes or the Valsalva maneuver associated with defecation and coughing.
The baroreceptor reflex however fails if the change in pressure is slow and sustained. This is because of baroreceptor resetting, wherein the baroreceptor adjusts itself to a different ‘resting’ blood pressure. The reset baroreceptor reflex then tries to maintain blood pressure at the new resting blood pressure. Because of baroreceptor resetting, this reflex is useless for the long-term regulation of blood pressure.
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The capillary fluid shift mechanism regulates blood pressure by filtering out more fluid into the interstitial spaces when the blood pressure rises. Conversely, when the blood pressure falls, interstitial fluid moves into the capillaries and opposes the fall in blood pressure.
The stress-relaxation mechanism is based on the plasticity of vascular smooth muscles. When there is a sustained increase in arterial blood pressure, the arterial and arteriolar smooth muscles
yield to the sustained distending pressure, leading to a dilatation of these vessels. This leads to an increase in the capacity of the arterial system with a concomitant fall in blood pressure. Pressure diuresis and natriuresis together constitute the most effective mechanism of long term regulation of blood pressure.
Whenever blood pressure increases, there is increased output of salt and water in urine. The consequent reduction in body fluid and electrolytes restores the blood pressure to normal. The renin-angiotensin mechanism is activated by sympathetic discharge. When blood pressure falls, it results in reflex increase in sympathetic discharge. The sympathetic discharge to the kidneys causes renin-degranulation. Renin catalyzes the formation of angiotensin I which is further converted into angiotensin II by angiotensin-converting enzyme (ACE).
Angiotensin II is a .powerful vasoconstrictor and therefore helps to restore blood pressure by increasing the peripheral resistance. Angiotensin II also brings about an increase in blood volume. It thus increases the cardiac output which helps in restoring the blood pressure. The increase in blood volume is brought about in two ways. Angiotensin is a powerful stimulator of thirst. It leads to consumption of large volumes of water, leading to a rise in blood volume. Angiotensin also stimulates the secretion of aldosterone from the renal medulla. Aldosterone leads to fluid and water retention through renal mechanisms.