Vasopressin and arterial pressure regulation. Special lecture

Data from conscious rats, dogs, and humans show that plasma arginine vasopressin (AVP) begins to exert vasoconstrictor activity at concentrations in the same range as those associated with maximum antidiuretic activity. Minimum pressor responses are observed with elevated plasma AVP, due in part to decreases of cardiac output and in part to withdrawal of sympathetic neural tone to various regions of the systemic circulation. These responses appear to some extent to be species-dependent. In conscious dogs, but not in rats, the fall of cardiac output is mediated by AVP stimulation of baroreceptor reflex pathways. Studies in rats indicate that AVP inhibits the sympathetic nervous system by direct action on the central nervous system. No evidence was found for inhibition at peripheral sites such as autonomic ganglia or vascular smooth muscle receptors. Also, AVP plays an important role in the regulation of arterial pressure with blood loss by direct vasoconstriction and by AVP enhancement of the strength of the baroreceptor reflex responses. The role of AVP in the long-term control of arterial pressure and in hypertension remains controversial, but plasma AVP is elevated in many experimental and human forms of hypertension. The link between plasma AVP and hypertension remains unclear because long-term elevation of AVP alone cannot sustain volume expansion or hypertension, and excess AVP does not enhance hypertension produced by sodium-retaining hormones or other vasoconstrictor agents. It appears that AVP plays mainly a permissive role by its fluid-retaining effects in most forms of hypertension. It is also possible that it acts as a central nervous system neural transmitter and modifies autonomic pathways in some forms of hypertension.