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Captopril (SQ 14225), a converting enzyme inhibitor, significantly lowered the arterial pressure (AP) of rats with angiotensin-salt hypertension, a hypertensive state associated with sodium retention, volume expansion, and suppression of both renin and aldosterone secretion. While captopril was acting, there was no increase in sodium, potassium, or water excretion. Thus, the antihypertensive effect was not due to natriuresis or diuresis. Moreover, as the AP was lowered, there was no change in plasma renin concentrtion, the pulse rate was lowered, and the lack of potassium retention suggested minimal or no effect on aldosterone secretion. The mechanism of action of captopril in a sodium-volume-expanded, renin-aldosterone-suppressed state is unknown.
E E Muirhead, and
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January 1996,
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E E Muirhead, and
B Brooks, and
W L Brosius
January 1981,
Hypertension (Dallas, Tex. : 1979),
E E Muirhead, and
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August 1983,
Nihon yakurigaku zasshi. Folia pharmacologica Japonica,
E E Muirhead, and
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January 1980,
Clinical and experimental hypertension,
E E Muirhead, and
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June 1983,
Nihon Naibunpi Gakkai zasshi,
E E Muirhead, and
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W L Brosius
January 1984,
Contributions to nephrology,
E E Muirhead, and
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August 1989,
Behavioral neuroscience,
E E Muirhead, and
B Brooks, and
W L Brosius
August 1973,
Clinical science and molecular medicine. Supplement,
E E Muirhead, and
B Brooks, and
W L Brosius
September 2001,
Journal of hypertension,
E E Muirhead, and
B Brooks, and
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April 1982,
The Journal of practical nursing,
