Regulation of Adrenocortical Function by Vasopressin

Abstract

Accumulating data obtained from various animal species indicate that vasopressin (AVP) participates in the regulation of adrenocortical function. AVP doubled aldosterone and cortisol secretion but did not affect corticosterone secretion. Pharmacological studies indicate that the AVP receptors in the cortex belong to the V1 a subtype. Activation of V1 a receptors induces breakdown of membrane phosphoinositides, with subsequent accumulation of inositol phosphates and diacylglycerol. These effects occur after receptor binding, G-protein activation and coupling to a specific phospholipase C. Inositol trisphosphate, transiently produced, induces a rapid release of Ca2+ from intracellular stores. Diacylglycerol activates protein kinase C, which, together with calcium, is responsible for steroid secretion. The early events of AVP action are mediated by two types of G-proteins. One is coupled to phospholipase C, and insensitive to pertussis toxin (probably Gq/11) and a second one, which is inactivated by pertussis toxin (Gi protein), is involved in the stimulation of calcium influx. This Ca2+ influx pathway is very important, as no steroidogenic effect of AVP could be observed when experiments were performed in a calcium-free medium or in pertussis toxin-treated cells. Besides the pituitary, the adrenal is also a source for AVP production. Indeed, AVP is synthesized and secreted by chromaffin cells either present in the medulla or scattered throughout the cortex with a more prominent concentration in zona glomerulosa. AVP receptors are also present on chromaffin cells. However, in contrast to AVP receptors in the cortex, these mainly belong to the V1 b subtype, although V1 a receptors are also detected. The results summarized in this review conclusively indicate that AVP is one of the regulators of both cortex and medulla, an influence which may be mediated in part via pituitary AVP and in part via local production of AVP.

Effect of acute heat stress on rat adrenal glands: a morphological and stereological study

“…These cells are responsible for production of aldosterone (the salt-retaining hormone), whose physiological effects correspond to the hypothalamic hormone, vasopressin (AVP). This hormone, according to Gallo-Payet and Guillon (1998), can also stimulate cortisol secretion, but not that of corticosterone, which is the dominant glucocorticoid in rats. It was shown that under conditions of stress, both ACTH and AVP secretion was increased (Aguilera, 1996), and when ACTH was secreted in large amounts, such as in conditions of stress, it could also stimulate aldosterone secretion.…”

In vivo activation of insulin receptor tyrosine kinase by melatonin in the rat hypothalamus

“…Furthermore, other hormones that act through GPCRs, including angiotensin II (AII), vasopressin, and luteinizing hormone (LH) can induce tyrosine phosphorylation of cytoplasm proteins (Marrero et al 1995;Saad et al 1995;Velloso et al 1996;Gallo-Payet and Guillon 1998;Carvalho et al 2003). AII and LH activate the cytosolic protein tyrosine kinase Janus kinase 2 (JAK2) and probably use this kinase to induce intracellular protein tyrosine phosphorylation.…”

The vasopressin V1b receptor critically regulates hypothalamic-pituitary-adrenal axis activity under both stress and resting conditions

“…Our present study and a previous study (33) using mice lacking the Crhr1 gene clearly showed that AVP and CRH are potent direct stimulators of ACTH and predominantly, if not exclusively, regulate ACTH release from the pituitary. On the other hand, corticosterone secretion from adrenal glands is complexly regulated not only by ACTH, but also by other factors, including direct and indirect vasopressin effects (33). Our data obtained from V1bR -/-mutants show that ACTH release is more closely related to AVP stimulation than the corticosterone release.…”