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Regulation of vasopressin V 1b receptors in the anterior pituitary gland of the rat
Author(s) -
Aguilera Greti,
RabadanDiehl Cristina
Publication year - 2000
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1111/j.1469-445x.2000.tb00004.x
Subject(s) - vasopressin , arginine vasopressin receptor 1b , medicine , endocrinology , vasopressin receptor , arginine vasopressin receptor 2 , glucocorticoid receptor , receptor , biology , pituitary gland , glucocorticoid , hormone , antagonist
Vasopressin secreted by parvocellular neurones of the hypothalamic paraventricular nucleus modulates pituitary adrenocorticotrophic hormone (ACTH) secretion by acting upon vasopressin V 1b type receptors in the pituitary corticotroph coupled to phospholipase C. Regulation of V 1b receptors contributes to the adaptation of the hypothalamic‐pituitary‐adrenal (HPA) axis to stress, as evidenced by the correlation between vasopressin receptor number and pituitary ACTH responsiveness. V 1b receptor upregulation during chronic stress is associated with elevated circulating glucocorticoids and vasopressin expression in parvocellular neurones, suggesting that these factors control V 1b receptor expression. Removal of circulating glucocorticoids by adrenalectomy causes sustained vasopressin receptor downregulation, but reduces V 1b receptor mRNA only transiently. The latter effect is not mediated by increased corticotrophin‐releasing hormone (CRH) and vasopressin release, since it is not prevented by lesions of the hypothalamic paraventricular nucleus. Adrenalectomy causes sustained V 1b receptor loss in Brattleboro rats, which lack hypothalamic vasopressin, suggesting that vasopressin mediates V 1b receptor mRNA recovery. Exogenous glucocorticoid administration downregulates pituitary vasopressin binding but increases V 1b receptor mRNA and facilitates coupling of the receptor to phospholipase C, effects which may contribute to the refractoriness of vasopressin actions to glucocorticoid feedback. The lack of parallelism between changes in pituitary vasopressin binding and V 1b receptor mRNA levels during manipulation of the HPA axis indicates that V 1b receptor content depends on post‐transcriptional mechanisms rather than steady‐state V 1b receptor mRNA levels. These studies suggest that interaction between glucocorticoids and vasopressin plays an important role in regulating V 1b receptor mRNA expression during alterations of the HPA axis. In addition, the recent characterization of a major part of the V 1b receptor gene provides a basis for studying the molecular mechanisms regulating the V 1b receptor.