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Decreased Vascular Responsiveness Produced by Angiotensin‐Converting Enzyme Inhibitors in the Rat Isolated Kidney

The effects of three angiotensin converting enzyme (ACE) inhibitors — captopril, diacid, and teprotide — on renal rascular responses to graded (SO, 100, 200 ng) injections of norepinephrine (NE) were examined in rat isolated perfused kidneys, baring a mean basal perfusion pressure of 78±10 mm Hg. The minimum dose of captopril (0.05 μg/ml, low dose) that abolished the vasoconstrictor responses to 100 and 200 ng angiotensin I did not affect NE-induced renal rasoconstriction, whereas a dose 100 times greater (high-dose captopril, 5 μg/ml) reduced the vasoconstrictor action of NE. MK-421 diacid also at high dose (1 μg/ml), caused similar reductions in renal vasoconstrictor responses to NE. In contrast, a high dose of teprotide (50 μg/ml) did not affect renal vascular responsiveness to NE.The threshold dose of NE that released prostaglandins, measured by bioassay, was 50 ng. Indomethacin (1 μg/ml) prevented NE-induced release of prostaglandins but did not affect the ability of captopril to attenuate NE-induced vasoconstriction. We conclude that captopril and MK-421 diacid decreases vascular reactivity in the rat isolated kidney by a mechanism independent of ACE inhibition and unrelated to a prostaglandlndependent vascular mechanism. Moreover, the presence of a mercapto function in the ACE inhibitor is not essential since captopril, which has a sulfhydryl group, and MK-421 diacid, which lacks this group, have similar effects on renal vascular responsiveness. (Hypertension 4 (suppl II): II-80-II-85, 1982)