The influence of ACE-inhibition by captopril on renal formation and metabolism of angiotensins I and II in patients with renovascular hypertension.

Fourteen patients with hypertension of presumed renovascular etiology were studied by renal vein catheterization. Unilateral renin secretion was found in 8 patients. In 4 of these patients a positive veno-arterial difference of plasma angiotensin I concentration (PAI) across the affected kidney increased markedly after a single dose of captopril. Across the contralateral kidney the net veno-arterial PAI difference changed from about zero before captopril to clearly negative values after captopril. The PAI values in the remaining 4 patients, who were already on captopril before the catheterization, were similar to those observed after a single dose of captopril. In patients with bilateral renin secretion the renal veno-arterial PAI differences across the kidneys were positive or close to zero before captopril. After captopril both positive and negative veno-arterial differences of PAI were observed. The plasma angiotensin II concentrations decreased after captopril to low values. These low values together with extremely high PAI values demonstrate effective ACE-inhibition. A high generation rate of angiotensin I in the affected kidney in patients with unilateral renin secretion after captopril is probably explained by activation of the local renin secretion. The angiotensin I "consumption" in the contralateral kidney after captopril in spite of no angiotensin II formation suggests the presence of alternative degradation processes for angiotensin I in the human kidney.