The vasodepressor actions of the cyclic endoperoxides PGG2 and PGH2 were compared with those of their products PGD2 and PGE2 using anaesthetised normotensive and genetically hypertensive rats. Given into the aortic arch of normotensives PGE2 was approximately 6 times more potent than PGH2 and 11 times more potent than PGG2 and PGD2. Hypertensive animals were 1.5-10 times more sensitive than normotensives to the depressor effects of PGG2 and PGH2, but their sensitivity to either PGD2 or PGE2 was similar. Thus in hypertensives the endoperoxides may be converted more readily to PGE2 and other products. In both types of rat PGG2 and PGH2 given intravenously were as active or more active than after intra-arterial. Therefore PGG2 and PGH2 may be converted more readily to more active products during passage through the lungs but whereas small doses of PGE2 are almost completely eliminated large doses may saturate uplmonary removal mechanisms.
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