血液透析患者におけるangiotensin I 変換酵素阻害剤captoprilの急性降圧機序に関する検討

抄録

In order to assess the mechanism of the acute antihypertensive effect of captopril in patients on hemodialysis (HD), mean blood pressuse (MBP), plasma renin activity (PRA), plasma aldosterone concentration (PAC), serum angiotensin cenverting enzyme activity (ACE), plasma bradikinin concentration (PBK) and blood concentration of captopril (BSQ) were measured before and 1, 2, 4, 6 hours after the oral administration of 25 mg captopril in 10 patients on HD. ACE was markedly suppressed from 12.8±1.3 mU/ml to 7.8±1.6 mU/ml and MBP fell significantly from 117±6 mmHg to 102±5 mmHg 1 hour after the administration and these effects continued for 6 hours. PRA and PBK increased significantly from 1.7±0.8 ng/ml/hr to 3.1±1.6 ng/ml/hr and 29±5 pg/ml to 42±6 pg/ml respectively. PAC was reduced significantly from 154±44 pg/ml to 134±39 pg/ml. Changes in MBP (ΔMBP) was significantly correlated with basal PRA(r=-0.75, p<0.01), basal PAC (r=-0.69, p<0.05) and changes in PRA (r=-0.72, p<0.01) but not with basal PBK nor changes in PBK. Furthermore, ΔMBP was not correlated with basal ACE. The maximum BSQ was obtained 1 hour after the administration and it showed a delay in the disappearance, and there was no correlation between ΔMBP and BSQ. These results suggest that, even in patients on HD whose blood pressure is presumably associated with volume expansion, the acute antihypertensive effect of captopril is mainly dependent on the effect to renin-angiotensin-aldosterone (R-A-A) system rather than kinin system. In conclusion, R-A-A system may play an important role in the regulation of blood pressure in patients on HD.