Vasopressin Baroreceptors

Logically, ADH receptor antagonists, and ADH synthesis and release inhibitors can be effective aquaretics. ADH, 8-arginine vasopressin [113-79-17, is synthesized in the hypothalamus of the brain, and is transported through the supraopticohypophyseal tract to the posterior pituitary where it is stored. Upon sensing an increase of plasma osmolaUty by brain osmoreceptors or a decrease of blood volume or blood pressure detected by the baroreceptors and volume receptors, ADH is released into the blood circulation it activates vasopressin receptors in blood vessels to raise blood pressure, and vasopressin V2 receptors of the nephrons of the kidney to retain water and electrolytes to expand the blood volume. 

Vasopressin (antidiuretic hormone [ADH]) secretion increases in response to decreased blood volume and/or reductions in effective blood volume via a decrease in inhibitory tone from both low-pressure and high-pressure baroreceptors to the hypothalamus. The neuronal pathways that mediate hemodynamic regulation of... 

Unlike isoflurane, desflurane may stimulate the sympathetic nervous system at concentrations above 1 MAC. Sudden and unexpected increases in arterial blood pressure and heart rate have been reported in some patients, accompanied by increases in plasma catecholamine and vasopressin concentrations and increased plasma renin activity. These pressor effects may increase morbidity or mortality in susceptible patients. The mechanism of sympathetic activation is unclear but does not appear to be baroreceptor-mediated. Clonidine, esmolol, fentanyl and propofol partially block the response but lignocaine (lignocaine) is ineffective. 

Vasopressin also plays an important role in the short-term regulation of arterial pressure by its vasoconstrictor action. It increases total peripheral resistance when infused in doses less than those required to produce maximum urine concentration. Such doses do not normally increase arterial pressure because the vasopressor activity of the peptide is buffered by a reflex decrease in cardiac output. When the influence of this reflex is removed, eg, in shock, pressor sensitivity to vasopressin is greatly increased. Pressor sensitivity to vasopressin is also enhanced in patients with idiopathic orthostatic hypotension. Higher doses of vasopressin increase blood pressure even when baroreceptor reflexes are intact. 

Thrasher TN. Baroreceptor regulation of vasopressin in renin secretion Low pressure vs. high pressure receptors (Review). Front Neuroendocrinol 1994 15 157-96. 

The neuronal pathways that mediate hemodynamic regulation of vasopressin release are different from those involved in osmoregulation. Baroreceptors in the left atrium, left ventricle, and pulmonary veins sense blood volume (filling pressures), and baroreceptors in the carotid sinus and aorta monitor arterial blood pressure. Nerve impulses reach brainstem nuclei predominantly through the vagal trunk and glossopharyngeal nerve these signals ultimately are relayed to the SON and PVN. 

Baroreceptors sensitive to the changes in blood pressure and transmitting their information to the hypothalamus and leading to the release of vasopressin are also suspected to exist. Their exact location is not known. The thyrocarotid junction and the carotid sinus have been suspected to be sites of such receptors. It cannot be excluded that the block of carotid circulation that leads to release of vasopressin is mediated by a decrease of cerebral flow or pressure rather than by a genuine baroreceptor reaction in the carotid circulation. The baroreceptor effect can only be demonstrated after vagotomy. 

It is not known how the volume receptor and the baroreceptor interact to regulate the secretion of vasopressin. 

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