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Blood pressure effects of endogenous brain angiotensin in rats are increased by inhibition of prostaglandin biosynthesis.

1. In Sprague—Dawley rats experiments were carried out to evaluate the influence of prostaglandins (PG) on the local generation of angiotensin (ANG) from brain angiotensinogen in cerebrospinal fluid and on the blood pressure effects of brain ANG. 2. In rats, pretreated with the PG biosynthesis inhibitor indomethacin (5 mg/kg subcutaneously every other day for 10 days), hog kidney renin was injected in doses of 0·001, 0·01 and 0·1 unit into the lateral brain ventricle. 3. At 15 min after the renin injections cerebrospinal fluid concentrations of ANG I and ANG II were markedly increased in a dose-dependent manner in the indomethacin-treated and in the untreated groups. At 60 min after the injection of renin ANG I concentrations decreased in both groups. However, the fall in ANG I in cerebrospinal fluid was more marked in indomethacin-pretreated animals. 4. Renin in doses of 0·001, 0·01 and 0·1 unit was injected into the lateral brain ventricles of unanaesthetized normotensive rats. A dose-dependent, long-lasting (> 2 h) increase in blood pressure of 9, 15 and 20% was observed. In conscious rats pretreated with indomethacin the blood pressure effects of the renin were greater (12, 23, 27%) when compared with results for untreated controls. 5. Intracerebroventricular injection into conscious rats of the ANG II antagonists [Sar 1 , Val 5 , Ala 8 ]ANG II and [NSuc 1 , Val 5 , Phg 8 ]ANG II in doses of 1 and 10 μg/kg reduced or abolished the renin-induced increases in blood pressure. 6. The results demonstrate that ANG I as well as ANG II are generated from brain angiotensinogen. The endogenously formed ANG II increases arterial blood pressure. This effect can be inhibited by brain intraventricular administration of specific ANG II antagonists, but it can be increased by inhibition of prostaglandin biosynthesis.