AJP - Regulatory, Integrative and Comparative Physiology, Vol 252, Issue 1 73-R77, Copyright © 1987 by American Physiological Society
Central angiotensin II and PGE2 act independently to increase blood pressure in conscious sheep
B. A. Breuhaus and J. E. Chimoskey
Conscious adult female sheep chronically prepared with nonocclusive
indwelling vascular and cerebroventricular catheters were used to determine
whether centrally administered prostaglandin E2 (PGE2) increases blood
pressure by activation of the brain renin angiotensin system or whether
centrally administered angiotensin II (ANG II) increases blood pressure by
stimulating prostaglandin synthesis in the brain. Intracerebroventricular
(ivt) ANG II, 50 ng X kg-1 X min-1, increased arterial pressure 23 mmHg (P
less than 0.01) 30 min after the start of infusion. Infusion of the ANG II
antagonist [Sar1-Thr8]ANG II (sarthran), 1,000 ng X kg-1 X min-1 ivt, had
no effect on arterial pressure when given by itself but reduced the ivt ANG
II-induced pressor response to 5 mmHg (P less than 0.05) when the two
peptides were infused at the same time. Intracerebroventricular infusion of
sarthran did not alter the pressor responses to intracarotid (ic) PGE2 or
to ivt PGE2. Blood pressure increased 21 mmHg (P less than 0.01) 30 min
after the start of PGE2 infusion when PGE2 was given ic by itself, compared
with 17 mmHg (P less than 0.01) when PGE2 was given ic at the same time as
sarthran was given ivt. Blood pressure increased 14 mmHg (P less than 0.01)
30 min after the start of PGE2 infusion when PGE2 was given ivt by itself,
compared with 16 mmHg (P less than 0.01) when PGE2 was given ivt at the
same time as sarthran was given ivt. Pretreatment with the cyclooxygenase
inhibitors indomethacin, 4 mg/kg sc, or flunixin meglumine, 3 mg/kg iv, did
not alter the ivt ANG II-induced pressor response.(ABSTRACT TRUNCATED AT
250 WORDS)
