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Hemodynamic effects of captopril in essential hypertension, renovascular hypertension and cardiac failure: Correlations with short- and long-term effects on plasma renin

1982; Elsevier BV; Volume: 49; Issue: 6 Linguagem: Inglês

10.1016/0002-9149(82)90360-5

1879-1913

G. J. Wenting, J. H. B. de Bruyn, A. J. Man inʼt Veld, A. J. J. Woittiez, F. H. M. Derkx, Maarten A.D.H. Schalekamp,

Sodium Intake and Health

The hemodynamic effects of captopril were investigated in 22 patients with essential hypertension, 22 with hypertension and renal artery stenosis and 14 with refractory chronic heart failure. The effects of a first dose of captopril, 50 mg orally, were observed for 2 hours, and the effects of repeated doses, 450 mg/day in combination with mild dietary sodium restriction, for at least 4 weeks. Short-term captopril treatment caused similar reductions in blood pressure in the three patient groups, that is, 21 ± 3 mm Hg in essential hypertension, 29 ± 6 mm Hg in renovascular hypertension and 21 ± 2 mm Hg in heart failure (mean ± standard error of the mean) despite large differences in pretreatment plasma renin. Heart rate and cardiac output did not change in hypertensive patients, and cardiac filling pressures decreased. The changes in right atrial pressure, pulmonary artery pressure and pulmonary capillary wedge pressure in essential hypertension and in renovascular hypertension did not differ. Heart rate decreased and cardiac output increased in heart failure, whereas cardiac filling pressures decreased. Blood pressure responses to long-term captopril therapy in essential and in renovascular hypertension were similar and, as with short-term treatment, changes in blood pressure were largely determined by changes in peripheral resistance. Several measurements of extracellular fluid volume showed no evidence of fluid retention by the kidneys. Short-term but not long-term blood pressure responses were correlated with pretreatment plasma renin (percent change in mean arterial pressure, short-term, versus log renin, r = 0.47, p < 0.001, n = 14). Both short- and long-term responses of total peripheral resistance were correlated with plasma renin (percent change in resistance, short-term versus log renin, r = 0.64, p < 0.001, n = 40; percent change in resistance, long-term versus log renin, r = 0.56, p < 0.001, n = 31). The correlations were weak and probably not important for clinical practice. These data indicate that other factors besides circulating renin are important in captopril's hypotensive effect. The favorable hemodynamic effects of converting enzyme inhibition warrant further consideration of this principle of therapy in the clinical management of most forms of hypertension and also in the treatment of chronic heart failure.