Hemodynamic and endocrine changes associated with captopril in diuretic-resistant hypertensive patients.

To evaluate the therapeutic efficacy of oral angiotensin-converting enzyme inhibition with low-dose (average 30 mg/day) captopril in diuretic-resistant hypertension, its long-term cardiocirculatory action was determined by dye-dilution method and venous-occlusion forearm plethysmography in 11 uncontrolled patients taking a thiazide diuretic. Significant declines in mean blood pressure (average 12.4 +/- 1.4 percent) and systemic vascular resistance (28.7 +/- 3.2 percent) accompanied an increase in cardiac output (24.8 +/- 4.1 percent). Forearm vascular resistance (16.0 +/- 2.7 percent) decreased considerably, but the decrease in limb vascular resistance did not parallel the fall in systemic vascular resistance in magnitude (p less than 0.01), indicating that arteriolar dilatation occurred on a selective basis. Plasma renin activity increased after therapy as plasma aldosterone levels consistently fell, while plasma norepinephrine concentrations were not changed. There was a direct correlation between pretreatment plasma renin activity and the magnitude of the decline in systemic vascular resistance (p less than 0.05). These findings suggest that the inhibition of angiotensin-converting enzyme with captopril in diuretic-resistant hypertensive patients improves cardiocirculatory function through selective dilatation. The reordering of regional blood flow, which appears to result from release of angiotensin-mediated vasoconstriction as well as the suppression of aldosterone, may underlie the prolonged benefit observed in these patients. This oral vasodilator in very low dose appears to represent an effective adjunct for the treatment of hypertension refractory to diuretics.