Mechanisms of central prostaglandin E2 hypertension in conscious dogs, sheep, and calves.

Intracarotid prostaglandin E2 (PGE2) infusions (10 ng X kg-1 X min-1) increased arterial pressure in conscious dogs, sheep, and calves. Total and regional peripheral resistances (renal, superior mesenteric, and iliac) increased in conscious calves. Arterial pH and CO2 tension did not change, implying no activation of the chemoreflex. The arterial baro-reflex was reset upward during intracarotid PGE2 infusion; arterial pressure increased with little heart rate change, but baroreflex sensitivity was unchanged. In contrast, equipotent intracarotid angiotensin II infusions (10 ng X kg-1 X min-1) both reset the baroreflex upward and decreased baroreflex sensitivity. Pretreatment with alpha-, but not beta-, adrenoceptor blocking agents attenuated the intracarotid PGE2 pressor effect. Increasing PGE2 infusions (10-200 ng X kg-1 X min-1) caused dose-related arterial pressure increases; plasma renin activity was increased only at the largest infusion rate. Pretreatment with captopril, an inhibitor of the angiotensin-converting enzyme, attenuated the PGE2 pressor effect. During barbiturate-halothane and chlorolose-urethan anesthesia, no pressor effect was observed during intracarotid PGE2. We conclude that intracarotid PGE2 acts centrally to augment sympathetic vasomotor outflow. The central action of PGE2 is not affected by activation of the arterial chemoreflex or alteration of baroreflex sensitivity and has a small renin-angiotensin component.