Arginine vasopressin (AvP)

The AVP, also termed as antidiuretic hormone (ADH), is secreted in reaction to an increase in extracellular fluid osmolality or decreased blood volume. It raises the water permeability of nephron gathering ducts, thereby promoting water re-absorption. These decreases extracellular fluid osmolality and urine output (i.e., an antidiuretic effect) therefore restoring blood volume. Therefore, AVP acts as a negative feedback regulator, defending set points in blood volume and body fluid osmolality.

The stores of AVP in the posterior lobe are big, enough to maintain maximum antidiuresis during numerous days of dehydration. The osmoreceptors that respond to changes in osmolality are in the vascular organ of the lamina terminalis (OVLT), one of the circum-ventricular organs of the brain that lie on the blood side of the blood–brain barrier. Osmolality-sensitive neurons in the OVLT synapse with the PVN and SON cells which are as shown in figure below and raise their firing rate as osmolality rises.

Figure: Position of the circumventricular organs (CVOs, shaded) in the rat brain (midsagittal portion); the ventricles are stippled.

A decrease in blood volume (i.e., hypovolemia) greater than around 10% (i.e., caused by dehydration or hemorrhage) stimulates the AVP secretion. The two mechanisms operate is as follows:

- Hypovolemia lowers the mean arterial blood pressure. This is observed by stretch receptors (i.e., baroreceptors) in the walls of the carotid sinus and aorta. The afferents of such pressure sensors run in the glossopharyngeal (IX) and vagus (X) cranial nerves to the nucleus of the solitary tract (NST) in the medulla. The NST starts noradrenergic neurons in the ventrolateral medulla that plan to the PVN and SON to bring around AVP discharge. A decreased blood pressure causes decreased firing of the baroreceptor afferents and therefore disinhibition of the circuitry triggering AVP secretion. This is as shown in the figure below.

Figure: A model for neural control of arginine vasopressin (AVP) secretion. The increased osmolality detected by the vascular organ of the lamina terminalis (OVLT) stimulates supraoptic and paraventricular nuclei (SON & PVN) cells to secrete AVP. The reduced arterial blood pressure is signaled through the nucleus of the solitary tract (NST) and the ventrolateral medulla (VLM) to the SON/PVN.

- Activation of the renin–angiotensin cascade is as shown in figure below. Renin is secreted by the juxtaglomerular apparatus (JGA) of the kidney in response to numerous factors contingent on a fall in blood volume.

       Figure: The renin–angiotensin cascade helps to maintain body fluid osmolality and blood volume.

Renin is a proteolytic enzyme that cleaves a plasma protein, angiotensinogen, to result a decapeptide, angiotensin I. This is more cleaved by angiotensin transforming enzyme (ACE), expressed on pulmonary endothelial cells, to the octapeptide, angiotensin II. Angiotensin II stimulates the subfornical organ (i.e., a circumventricular organ), neurons of that stimulate AVP secretion. Additionally, AII stimulates vasoconstriction, drinking, and the secretion of aldosterone; all actions that help restore blood volume and pressure.