Area postrema lesions augment the pressor activity of centrally administered vasopressin.

The effects of arginine vasopressin given into either the vertebral arteries, a peripheral vein (IV), or the cisterna magna of 15 morphine-chloralose anesthetized dogs were measured before and after pharmacological blockade with the antagonist [d(CH2)5 Tyr(Me) AVP]. The contribution of the area postrema to the pressor activity of vasopressin was assessed in nine other dogs by comparing the responses to vasopressin before and after surgical ablation of this structure. Administration of vasopressin either via the vertebral arteries or intravenously produced comparable gradual rises in blood pressure, accompanied by bradycardia and decreases in the plasma levels of norepinephrine. Administration of intracisternal vasopressin elicited a smaller rise in arterial pressure, tachycardia, and increases in plasma norepinephrine levels. The pressor and bradycardic effects of IV vasopressin were abolished when the antagonist was given via the same route. In contrast, intravertebral infusion of the vasopressin antagonist caused tachycardia and modest hypotension in response to intravenous or intravertebral infusions of vasopressin. Pressor effects of vasopressin given into the cisterna magna were not altered by systemic delivery of the vasopressin blocker. Removal of the area postrema selectively augmented the pressor effects of intravertebral vasopressin, whereas the pressor activity of IV vasopressin remained unchanged. These findings provide new evidence for an action of circulating vasopressin in cardiovascular regulation, mediated in part by the area postrema.