Attenuated stress-induced catecholamine release in mice lacking the vasopressin V_1b receptor

Abstract

. Attenuated stressinduced catecholamine release in mice lacking the vasopressin V1b receptor. Am J Physiol Endocrinol Metab 291: E147-E151, 2006. First published February 7, 2006 doi:10.1152/ajpendo.00005.2006.-Vasopressin V1b receptor is specifically expressed in the pituitary and mediates adrenocorticotropin release, thereby regulating stress responses via its corticotropin releasing factor-like action. In the present study we examined catecholamine release in response to two types of stress in mice lacking the V1b receptor gene (V1bR Ϫ/Ϫ mice) vs. wild-type mice. There were no significant differences in the basal plasma levels of catecholamines between the two genotypes. In response to stress induced by forced swimming, norepinephrine (NE), but not epinephrine (E) or dopamine (DA), was increased in wild-type mice, whereas the increases in NE and DA were not observed in V1bR Ϫ/Ϫ mice. In wild-type mice, E, but not NE or DA, was increased in response to social isolation stress, whereas the increase in E was not observed in V1bR Ϫ/Ϫ mice. These results suggest that the V1b receptor regulates stress-induced catecholamine release. Because it has been suggested that arginine-vasopressin (AVP) is related to the development of depression, we also evaluated immobility time in the forced swimming test, and we found no significant change in V1bR Ϫ/Ϫ mice. Taken together, these findings suggest that, in addition to the previously elucidated effect on the hypothalamic-pituitary-adrenal axis, vasopressin activity via V1b receptors regulates stress-induced catecholamine release.V1b receptor knockout mice; norepinephrine; epinephrine; dopamine; immobility time in the forced swimming test ARGININE VASOPRESSIN (AVP) has diverse physiological functions, and these physiological effects are mediated through the binding of AVP to specific receptor subtypes of the target cells. AVP receptors are G protein coupled and are divided into at least three types (V 1a , V 1b , and V 2 ). The V 1a (vascular/hepatic) and V 1b (anterior pituitary) receptors act via phosphatidylinositol hydrolysis and Ca 2ϩ mobilization (9). The V 1a receptor mediates physiological effects such as smooth muscle cell contraction and proliferation, platelet aggregation, and glycogenolysis. The V 1b receptor exists in the anterior pituitary, where it stimulates corticotropin release. The V 2 receptor is found primarily in the kidney and mediates the antidiuretic effect of AVP via adenylate cyclase/cyclic AMP signals (20) and aquaporin 2 trafficking (15). All of these receptors have been cloned (11,12,13) and belong to the family of seven membrane-spanning G protein-coupled receptors.AVP is synthesized primarily in the magnocellular neurons of the hypothalamic paraventricular nuclei (PVN) and in the supraoptic nuclei that project to the posterior pituitary. In addition, parvocellular neurons of the PVN coexpressing AVP and corticotropin-releasing hormone (CRH) coordinate hypothalamic-pituitary-adrenal (HPA) system activity and project to the external layer of th...

Vasopressin: Behavioral roles of an “original” neuropeptide

“…The normal catecholamine release in response to stress is decreased in Avpr1b −/− males, particularly release of epinephrine (Itoh et al, 2006). As noted above, no differences in circulating ACTH and corticosterone levels between Avpr1b KO and wildtype mice have been found (Wersinger et al, 2002;Lolait et al, 2007a).…”

Vasopressin V1a and V1b Receptors: From Molecules to Physiological Systems

“…Chronic isolation stress increased plasma catecholamine levels in WT mice, as observed in rats (31), but not in V1bR-KO mice (244). When animals were exposed to acute forced swimming stress, the blood epinephrine level was significantly increased in WT mice, but less so in V1bR-KO mice (244). These results suggest that the AVP/V1b receptor pathway may participate in the regulation of plasma catecholamine levels by directly promoting catecholamine release by the adrenal medulla under stress conditions in vivo.…”

“…The functional role of the V1b receptor in the adrenal medulla under stress conditions was investigated by analyzing the plasma catecholamine levels in V1bR-KO mice. Basal plasma levels of catecholamine such as epinephrine, NE, and dopamine (DA) did not differ between WT and V1bR-KO mice (244). Chronic isolation stress increased plasma catecholamine levels in WT mice, as observed in rats (31), but not in V1bR-KO mice (244).…”

“…Basal plasma levels of catecholamine such as epinephrine, NE, and dopamine (DA) did not differ between WT and V1bR-KO mice (244). Chronic isolation stress increased plasma catecholamine levels in WT mice, as observed in rats (31), but not in V1bR-KO mice (244). When animals were exposed to acute forced swimming stress, the blood epinephrine level was significantly increased in WT mice, but less so in V1bR-KO mice (244).…”

“…The relevance of these findings in a clinical setting needs to be further explored. The V1b receptors, on the other hand, mediate ACTH secretion by the anterior pituitary and also mediate catecholamine release from the adrenal medulla (244). Whether these V1b receptors participate in the regulation of cardiovascular function by AVP remains to be determined.…”