Modifications by endogenous prostaglandins of angiotensin II-induced contractions in dog and monkey cerebral and mesenteric arteries.

In monkey and dog cerebral artery strips, angiotensin (ANG) II (10(-7) M) produced a transient contraction, which was abolished or suppressed by treatment with indomethacin, aspirin, ONO3708, diphloretin phosphate, antagonists of prostaglandins (PGs) and OKY046, a thromboxane A2 synthesis inhibitor, and by endothelium denudation. On the other hand, PGF2 alpha-induced contractions were not influenced by indomethacin and aspirin, but were suppressed by treatment with ONO3708 and OKY046. Treatment with indomethacin or aspirin potentiated the contractile response of monkey mesenteric arteries, whereas treatment with ONO3708 and removal of endothelium did not alter the response significantly. Saralasin abolished the response to ANG II in these arteries. These findings may indicate that ANG II contracts monkey and dog cerebral arteries by activation of ANG II receptors mainly in endothelium, releasing arachidonic acid and synthesizing vasoconstrictor PGs, such as PGF2 alpha, E2, A2 and D2. Involvement of thromboxane A2 is if any minimal. Vasoconstrictor and dilator PGs released by ANG II appear to modify differently the contraction caused by direct actions of the octapeptide on smooth muscle in monkey cerebral and mesenteric arteries.