The effect of a vasopressin antagonist on the pressor response to histamine administered centrally.

The mechanism for the pressor response to intracerebroventricularly (i.c.v.) administered histamine was studied. Histamine (HA), when injected intracerebroventricularly in rats, produced a dose-dependent increase in mean arterial pressure (MAP) which was subject to tachyphylaxis. Spinal transection at C-7 in the anesthetized rat did not attenuate the rise in blood pressure. The possibility that the release of 8-arginine vasopressin was responsible for the rise in blood pressure was explored. By pretreating conscious freely-moving rats with a specific antagonist to the vasopressor action of vasopressin viz., [1-beta-mercapto-beta, beta-cyclopentamethyleneproprionic acid), 2-(O-methyl) tyrosine] arginine-vasopressin, there was a statistically-significant attenuation of the pressor response to intracerebroventricularly administered histamine. The antagonist however, did not totally abolish the pressor response, regardless of the dose employed. Concomitant administration of hexamethonium and the vasopressin antagonist did not further attenuate the response. Previous adrenal demedullation did not diminish the response to intracerebroventricularly administered histamine, nor was there any evidence for release of angiotensin II since pretreatment with saralasin did not attenuate the cardiovascular response. These findings suggest that vasopressin along with other as yet undefined substances, are released from the central nervous system to produce the increase in blood pressure after intracerebroventricularly administered histamine.