Central role for vasopressin in cardiovascular regulation and the pathogenesis of hypertension.

In recent years the role of neuropeptides in the central regulation of arterial pressure and the pathogenesis of hypertension has been the subject of considerable attention. Of all the neuropeptides, vasopressin (AVP) has been one of the most widely studied. The availability of sophisticated immunocytochemical and biochemical methods has permitted localization of AVP in areas of the brain known to be involved in cardiovascular regulation. In addition, specific AVP receptors with high affinity have been found in these brain areas. Several lines of evidence suggest that central AVP plays a role in the control of blood pressure and heart rate in both normotensive and hypertensive animals. Administration of AVP into the central nervous system produces changes in arterial pressure and heart rate that can be reversed by competitive antagonists. AVP interacts with neurotransmitters such as catecholamines, which are involved in arterial pressure regulation. It is also a potent releasing factor for adrenocorticotropic hormone (ACTH)-corticosterone, which in turn acts on the cardiovascular system. Agents that inhibit the interaction of AVP with its receptors have cardiovascular effects. Furthermore, levels of AVP and its receptor are altered in hypertensive states. Finally, increased sensitivity to the pressor effects of AVP has been described in experimental models of hypertension. This review will focus on evidence for a central role for AVP in cardiovascular regulation and the pathogenesis of hypertension, and discussion will mainly focus on work done in rats. It should be noted that there is increasing evidence for species differences in responsiveness to AVP and mechanisms of action of AVP. For a more detailed discussion of the neuroanatomy, biochemistry, molecular biology, and physiology of this peptide,