Mechanism
There are several mechanisms through which the body regulates arterial pressure.
Baroreceptor Reflex
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In response to acute changes in blood pressure, the body responds through the baroreceptors located within blood vessels. Baroreceptors are a form of mechanoreceptor that become activated by the stretching of the vessel. This sensory information is conveyed to the central nervous system and used to influence peripheral vascular resistance and cardiac output.
There are two forms of baroreceptors.
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High-Pressure Baroreceptors
Two baroreceptors are located within the high-pressure arterial system.
These both send signals in response to the physical distortion of the vessel. The stretch of the vessel leads to an increase in action potential relayed from the sensory endings located in the tunica adventitia of the artery. These action potentials get transmitted to the solitary nucleus that signals to autonomic neurons secrete hormones to affect the cardiovascular system. Activation of the aortic baroreceptor during increases in blood pressure effectively inhibits the efferent sympathetic nerve response.[5] On the other hand, if an individual’s blood pressure were to fall such as in hypovolemic shock, the rate of action potential from the baroreceptors would be decreased due to reduced depolarization; this would lead to reduced inhibition of sympathetic activity, resulting in a reflex to increase pressure.
Low-Pressure Baroreceptors
These baroreceptors are present within the low-pressure venous system. They exist within large veins, pulmonary vessels, and within the walls of the right atrium and ventricle. The venous system has compliance approximately 30 times greater than that of the arterial system [6]. Changes in volume largely influence the baroreceptors in the venous system. Decreased frequency in action potentials in low-pressure scenarios leads to the secretion of antidiuretic hormone, renin, and aldosterone. These lead to a downstream effect to regulate arterial pressure.
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Antidiuretic Hormone
Antidiuretic hormone (ADH), also known as vasopressin, is a hormone synthesized in the magnocellular neurosecretory cells within the paraventricular nucleus and supraoptic nucleus of the hypothalamus. ADH is synthesized and released in response to multiple triggers which are:
The antidiuretic hormone produced in the hypothalamus makes its way down the pituitary stalk to the posterior pituitary where it is kept in reserve for release in response to the above-listed triggers. ADH mainly functions to increase free water reabsorption in the collecting duct of the nephrons within the kidney, causing an increase in plasma volume and arterial pressure. ADH in high concentrations has also been shown to cause moderate vasoconstriction, increasing peripheral resistance, and arterial pressure.[7][8]
Renin-Angiotensin-Aldosterone System (RAAS)
The renin-angiotensin-aldosterone system is an essential regulator of arterial blood pressure. The system relies on several hormones that act to increase blood volume and peripheral resistance. It begins with the production and release of renin from juxtaglomerular cells of the kidney. They respond to decreased blood pressure, sympathetic nervous system activity, and reduced sodium levels within the distal convoluted tubules of the nephrons. In response to these triggers, renin is released from the juxtaglomerular cells and enters the blood where it comes in contact with angiotensinogen which is produced continuously by the liver. The angiotensinogen is converted into angiotensin I by renin. The angiotensin I then make its way to the pulmonary vessels, where the endothelium produces the angiotensin-converting enzyme (ACE). Angiotensin I is then converted to angiotensin II by ACE. Angiotensin II has many functions to increase arterial pressure, including:
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