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依那普利对缺钠大鼠血管紧张素转换酶的影响

Angiotensin-converting enzyme responses following enalapril in the sodium deficient rat.

作者信息

Longman S D, Howlett D R

出版信息

Eur J Pharmacol. 1986 Apr 29;123(3):379-86. doi: 10.1016/0014-2999(86)90712-0.

Abstract

The relationship between blood pressure lowering activity and inhibition of plasma and tissue angiotensin-converting enzyme (ACE) has been studied in the sodium deficient normotensive rat at 24, 48 and 96 h after the administration for 21 days of enalapril (MK-421, 10 mg/kg per day p.o.). Blood pressure was reduced and plasma ACE activity inhibited at 24 and 48, but not 96 h, after cessation of dosing. Tissue ACE activity (aorta, lung, mesenteric bed) was inhibited up to 96 h post dose when blood pressure had returned to control values. ACE production (activity following removal of inhibitor) was increased in plasma at 24, 48 and 96 h post dose but in tissues (adrenal glands, renal arteries and mesenteric bed) only at 48 h post dose. There was no tendency for ACE production to increase in the lung, the largest source of the enzyme in the rat. Thus it appears that inhibition of ACE activity in both plasma and tissue contributes to the blood pressure lowering activity of enalapril in the sodium deficient normotensive rat.

摘要

在给正常血压的缺钠大鼠口服依那普利(MK - 421,每天10毫克/千克)21天后,分别于停药后24、48和96小时研究了血压降低活性与血浆及组织血管紧张素转换酶(ACE)抑制之间的关系。停药后24和48小时血压降低且血浆ACE活性受到抑制,但96小时时未出现此情况。给药后长达96小时,当血压恢复到对照值时,组织ACE活性(主动脉、肺、肠系膜床)受到抑制。给药后24、48和96小时血浆中ACE生成(去除抑制剂后的活性)增加,但仅在给药后48小时组织(肾上腺、肾动脉和肠系膜床)中ACE生成增加。在大鼠体内该酶的最大来源——肺中,ACE生成没有增加的趋势。因此,似乎血浆和组织中ACE活性的抑制均有助于依那普利在缺钠正常血压大鼠中的降压活性。

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