Receptors Mediating the CRH Effects of Vasopressin and Oxytocina

Abstract

The data highlighted here suggest that the CRH effects of vasopressin and oxytocin are mediated by one and the same hypophysial receptor which has unique pharmacological specificity. The nomenclature for this receptor type is not established; both V3(53) and V1 beta 39 have been proposed. The former proposal is logical if the pharmacology of ligand recognition is emphasized, whereas the latter designation takes into account that transmembrane signalling from V1 receptors occurs via coupling proteins Go and Gi but not Gs. Such issues are best resolved after cDNA cloning of the genes for the receptors: in the meanwhile the working definition V3 seems more convenient. Several studies show that pituitary V3 receptors are regulated by the concentration of vasopressin in hypophysial portal blood and the amount of glucocorticoid hormones in the circulation (see Ref. 9 for review). Work in this area should clarify further the intracellular mechanism of the CRH action of vasopressin, as well as the factors that determine the responsiveness of corticotrophs to various secretagogues. Most recently, it has been shown that vasopressin is a potent thyrotropin-releasing hormone. This finding extends further the growing concept that there is considerable "cross-talk" between the classical neuroendocrine axes. These were previously thought to be separated by the hypothalamic organization of "final common pathways" of neuroendocrine motoneurons in the hypothalamus, each producing a unique neurohormone to regulate a single type of adenohypophysial cell. It seems that the days of the validity of this hypothesis are numbered, and an important task will be to determine the possible physiological significance of the "cross-talk" within the hypothalamo-pituitary unit in the regulation adrenocortical function.