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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. 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 . 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.

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:

1. High serum osmolarity, which acts on osmoreceptors in the hypothalamus
2. Low blood volume causes a decreased stretch in the low-pressure baroreceptors, leading to the
production of ADH
3. Decreased blood pressure causes decreased stretch in the high-pressure baroreceptors, also leading to the
production of ADH
4. Angiotensin II

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.

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:

• Potent vasoconstriction of arterioles throughout the body

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