AJP - Heart and Circulatory Physiology, Vol 247, Issue 2 218-H228, Copyright © 1984 by American Physiological Society
Mechanisms of central prostaglandin E2 hypertension in conscious dogs, sheep, and calves
S. S. Hull Jr and J. E. Chimoskey
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.
