ABSTRACT
Arginine-vasopressin (AVP), also known as antidiuretic hormone, is a peptide hormone that is synthesized by magnocellular neurons in the hypothalamus of the mammalian brain. One of vasopressin's primary functions, as its name implies, is to constrict the vasculature to elevate blood pressure (BP). Constriction of the splanchnic arterial vasculature can significantly increase total peripheral vascular resistance and provides a very effective mechanism for restoration of BP. At the level of the vasculature, the BP restoring actions of circulating AVP have been attributed to the vasoconstrictor effects elicited by binding of AVP to V1a-vasopressin receptors on vascular smooth muscle cells (VSMCs), particularly those located on the surface of arterial smooth muscle cells of the splanchnic circulation. The signal transduction pathways whereby binding of AVP to V1a receptors results in contraction of VSMCs had been extensively studied by the early to mid-1990s. Several methodological considerations were required to identify the vasoconstrictor signaling pathways that account for the physiological actions of circulating AVP.
