Arvola P, Nurmi A K, Säynävälammi P, Manninen V, Vapaatalo H
Department of Biomedical Sciences, University of Tampere, Finland.
Methods Find Exp Clin Pharmacol. 1989 Feb;11(2):67-71.
Blood pressure responses to the angiotensin-converting enzyme (ACE) inhibitor enalapril were investigated in rats with salt-dependent hypertension. In both one- and two-kidney deoxycorticosterone (DOC)-NaCl hypertension, enalapril (50 mg/kg p.o.) caused a similar, slight blood pressure fall, which passed off with continuation of the treatment. Changes in the salt concentration of the drinking fluid (from 1% NaCl to 0.2% NaCl in the one-kidney rats and from 1% NaCl to 2% NaCl in those with intact kidneys) did not alter the depressor effect of enalapril. Plasma renin activity in all DOC-NaCl hypertensive groups was negligible. Our results indicate that in DOC-NaCl hypertensive rats, the presence of intact kidneys vs. one kidney has no influence on the blood pressure response to ACE inhibition. The blood pressure-lowering effect of enalapril may result from local converting enzyme inhibition in tissues.
在盐依赖性高血压大鼠中研究了血管紧张素转换酶(ACE)抑制剂依那普利的血压反应。在单肾和双肾脱氧皮质酮(DOC)-氯化钠高血压模型中,依那普利(口服50mg/kg)引起相似的轻度血压下降,持续给药后血压下降消失。饮用液体的盐浓度变化(单肾大鼠从1%氯化钠变为0.2%氯化钠,双肾大鼠从1%氯化钠变为2%氯化钠)并未改变依那普利的降压作用。所有DOC-氯化钠高血压组的血浆肾素活性均可忽略不计。我们的结果表明,在DOC-氯化钠高血压大鼠中,双肾与单肾状态对ACE抑制的血压反应没有影响。依那普利的降压作用可能源于组织中局部转换酶的抑制。