Key result
Cyclooxygenase inhibitors attenuated angiotensin II-induced contractions in monkey coronary arteries, but potentiated them in renal arteries and prolonged them in mesenteric veins.
Cyclooxygenase products differentially modulate angiotensin II-induced vasoconstriction depending on the specific vascular bed in monkeys.
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Primate vascular data show bed-specific COX modulation of Ang II responses; hypothesis-generating and should not change practice.
In coronary, renal and femoral arteries and mesenteric veins isolated from Japanese monkeys, tachyphylaxis to angiotensin (ANG) II (10-7 M)-induced contraction rapidly developed. Contractions caused by ANG II in coronary arteries were attenuated by treatment with indomethacin and aspirin and also by endothelium denudation. Indomethacin inhibited the response of the arteries with and without endothelium to a similar extent. OKY 046, a thromboxane A2 synthesis inhibitor, failed to inhibit the response. In contrast, contractions of renal arteries were potentiated and prolonged by the cyclooxygenase inhibitors. ANG II-induced contractions of mesenteric veins were prolonged but those of femoral arteries were not altered by indomethacin. It is concluded that ANG II contracts monkey coronary arteries, possibly due to the release of vasoconstrictor prostanoids but not thromboxane A2 from endothelial and subendothelial tissues and also due to its direct action on smooth muscle, whereas contractions of renal arteries and mesenteric veins are blunted by vasodilator prostanoids, possibly PGI2. Cylooxygenase products even if released do not appear to regulate femoral artery contractions produced by ANG II.
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Yoshida et al. (1991) studied Isolated monkey arteries and veins. Cyclooxygenase inhibitors (indomethacin, aspirin) vs. Without inhibitors was evaluated on Angiotensin II-induced contraction. Cyclooxygenase inhibitors attenuated angiotensin II-induced contractions in monkey coronary arteries, but potentiated them in renal arteries and prolonged them in mesenteric veins.
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