Role of vasopressin in the control of arterial pressure

Elevations in the circulating levels of vasopressin within the physiological range (less than 30 fmol X mL-1) in conscious animals cause vasoconstriction of resistance vessels, the most profound effect occurring in the muscle, skin, and intestinal vascular beds. In the organism with normal baroreceptor function, the vasoconstriction is not expressed as an increase in arterial pressure because of a corresponding fall in cardiac output associated with enhanced cardiovascular reflex activity. When compensatory reflex mechanisms are impaired (baroreceptor-denervated dogs, patients with autonomic insufficiency, hypertensive rats), the vasoconstrictor activity of vasopressin is exposed and is reflected as an increase in arterial pressure. Inactivation of the vasopressin system alone by hypophysectomy or by administration of antagonists of the pressor activity of vasopressin is often accompanied by compensatory activation of the renin-angiotensin system. Thus, under certain conditions, the vasopressin system and the renin-angiotensin system operate as reciprocal or redundant mechanisms in the control of resistance vessels and of arterial pressure. In two rat models of hypertension (spontaneously hypertensive rats and DOC-salt hypertensive rats) plasma levels of vasopressin are elevated, inactivation of the vasopressin system lowers arterial pressure, and pressor responsiveness to the peptide is enhanced. The enhanced pressor responsiveness appears related in part to impaired reflex activity. The mechanism of the impaired reflexes is unknown but in spontaneously hypertensive rats it might be related to a vasopressin deficit in the paraventricular nucleus and brain stem. The evidence is consistent with the possibility that vasopressin is one factor among many that may play a role in the maintenance of arterial pressure in the adult spontaneously hypertensive rat and in the development and maintenance of the hypertensive state in DOC-salt hypertensive rats.