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血管紧张素I转换酶抑制剂(SQ 14,225)的血压与血药浓度之间的关系。

Relationship between blood pressure and blood levels of angiotensin I converting enzyme inhibitor (SQ 14,225).

作者信息

Honda M, Izumi Y, Kawahara Y, Hatano M

出版信息

Jpn Circ J. 1981 Sep;45(9):1025-9. doi: 10.1253/jcj.45.1025.

Abstract

The time courses of mean blood pressure (MBP), plasma renin activity (PRA), plasma aldosterone (PA), serum prostaglandin E (PGE), serum angiotensin I converting enzyme (ACE), and blood levels of angiotensin I converting enzyme inhibitor (SQ 14,225) (captopril) were studied in 6 patients with essential hypertension (5 men and 1 woman, aged 44 +/- 5.6 (mean +/- S.E.) years) before and 30, 60, 120 and 180 min after administration of 25 mg captopril. MBP and ACE began to fall within 30 min and reached a significant minimum between 60 and 180 min after captopril administration. PRA was significantly increased 60 min after captopril administration and continued for 180 min. On the other hand, PA had begun to fall significantly 180 min after captopril administration. The blood levels of captopril were significantly increased 30 min after captopril administration, with a peak at 120 min. The levels at 180 min were half the peak. The levels of PGE were not significantly changed within 180 min after captopril administration. These results suggest a discrepancy between the changes in MBP and the blood levels of captopril. The blood pressure lowering effect may be due to inhibition of angiotensin II (Ang. II) during the short-acting effect, and due to decrease of PA, metabolites of captopril, increase of kinin in the blood, inhibition of the slow pressor effect of Ang. II, increases of other depressor hormones such as prostacyclin and other depressor mechanisms during the long-acting effect.

摘要

对6例原发性高血压患者(5例男性,1例女性,年龄44±5.6(均值±标准误)岁)在服用25毫克卡托普利之前以及之后30、60、120和180分钟,研究了平均血压(MBP)、血浆肾素活性(PRA)、血浆醛固酮(PA)、血清前列腺素E(PGE)、血清血管紧张素I转换酶(ACE)以及血管紧张素I转换酶抑制剂(SQ 14,225)(卡托普利)的血药浓度的时间进程。服用卡托普利后30分钟内MBP和ACE开始下降,在60至180分钟之间降至显著最低值。服用卡托普利60分钟后PRA显著升高,并持续180分钟。另一方面,服用卡托普利180分钟后PA已开始显著下降。服用卡托普利30分钟后卡托普利的血药浓度显著升高,在120分钟时达到峰值。180分钟时的浓度为峰值的一半。服用卡托普利180分钟内PGE的水平无显著变化。这些结果提示MBP变化与卡托普利血药浓度之间存在差异。降压作用可能在短效作用期间归因于对血管紧张素II(Ang. II)的抑制,而在长效作用期间归因于PA的降低、卡托普利代谢产物的增加、血液中激肽的增加、对Ang. II缓慢升压作用的抑制、其他降压激素如前列环素的增加以及其他降压机制。

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