Okamura T, Yoshida K, Toda N
Department of Pharmacology, Shiga University of Medical Sciences, Ohtsu, Japan.
J Pharmacol Exp Ther. 1990 Jul;254(1):198-203.
In dog renal artery strips with intact and damaged endothelium, relaxations induced by angiotensin II possibly mediated via the release of prostaglandin (PG) I2 were abolished or reversed to contractions by treatment with methylene blue and indomethacin. Relaxations elicited by arachidonic acid were also inhibited markedly. PGH2-induced contractions in the arteries with endothelium were potentiated, and relaxations caused by PGH2 in the endothelium-denuded arteries were suppressed by methylene blue, whereas these responses were not influenced by indomethacin. Relaxant responses to PGI2 and beraprost, a stable analog of PGI2, were not reduced by methylene blue. The amount of 6-keto PGF1 alpha in the bathing media released from the renal artery was decreased by treatment with methylene blue and indomethacin, whereas amounts of PGE2 and thromboxane B2 were not influenced by methylene blue but were reduced by indomethacin. It may be concluded that methylene blue interferes with the synthesis and release of PGI2 in the dog renal arteries; therefore, the relaxation mediated by endogenous PGI2 is suppressed. However, methylene blue does not appear to inhibit the synthesis of other cyclooxygenase products.
