Abstract
In order to clarify the hypotensive mechanisms of converting enzyme inhibitor, captopril (50mg) was administered orally in 11 hypertensive patients, of whom 9 had essential hypertension, one had primary aldosteronism, and one had glucocorticoid responsive hyperaldosteronism. There was a significant correlation between fall in mean blood pressure (MBP) and pretreatment levels of plasma renin activity (PRA) at 30 min after captopril in 9 patients with essential hypertension (r=-0.687, p<0.05). On the other hand, there was also a significant correlation between the fall in MBP and changes in plasma bradykinin (BK) levels in response to captopril at 15 min (r=-0.753, p<0.02) and 120 min (r=-0.754, p<0.02) in essential hypertensives. In essential hypertensives with PRA above 1.5 ng/ml/h (group I), the decrease of plasma aldos-terone concentration (PAC) was significantly greater than those with PRA below 1.5 ng/ml/h (group II) at any time after captopril administration, while the increments in plasma BK of group I was lesser than those in group II. In a patient with primary aldosteronism, and also in a patient with glucocorticoid responsive hyperaldosteronism, captopril lowered markedly their blood pressures with a significant elevation of plasma BK, while both PRA and PAC were unchanged. From these findings, it is suggested that the hypotensive effect of captopril is mainly due to the inhibition of the renin-angiotensin-aldosterone system rather than that of the kallikrein-kinin axis in high-renin hypertension. Conversely, in low-renin hypertension, the hypotensive action may contribute to its inhibitory effect on the kallikrein-kinin system rather than that on the renin-angiotensin-aldosterone system.
