[Recent advances in vasopressin receptors and signal transduction system]

The antidiuretic hormone arginine vasopressin (AVP) receptors are G protein-coupled and have been divided into at least three types: V1a (vascular/hepatic) and V1b (anterior pituitary) receptors, which act through phosphatidylinositol hydrolysis to mobilize intracellular Ca2+; and V2 (kidney) receptor, which is coupled to adenylate cyclase. Recently V1a and V2 receptor cDNAs were cloned. These cDNAs encode proteins with seven putative transmembrane domains and a similar structure to rhodopsin and other G protein-coupled receptors. Micro-localization of mRNA coding for V1a and V2 receptors was carried out in the rat kidney using a reverse transcription and polymerase chain reaction. Large signals for V1a receptor PCR product were detected in glomerulus, cortical collecting duct (CCD), outer medullary collecting duct (OMCD), inner medullary collecting duct (IMCD), and arcuate artery. Large signals for V2 receptor PCR product were detected in CCD, OMCD, and IMCD. 72-hour dehydration caused decrease of V2 receptor mRNA, but no change in V1a receptor mRNA in rat IMCD. These data show that mRNA coding for the two AVP receptor subtypes are distributed differently along the nephron and renal vascular system, and that these mRNAs are regulated differently in response to the dehydrated state. Recently, two reports of a mutation in the vasopressin V2 receptor gene in a kindred with X-rinked nephrogenic diabetes insipidus are published. These studies demonstrated that point mutation of V2 receptor gene causes the nephrogenic diabetes insipidus. Understanding the nature of defective diabetes insipidus may ultimately lead to improved therapy.