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在肾灌注压降低期间,血管紧张素转换酶抑制可防止钠和水潴留以及平均动脉血压升高。

ACE inhibition prevents Na and water retention and MABP increase during reduction of renal perfusion pressure.

作者信息

Boemke W, Seeliger E, Rothermund L, Corea M, Pettker R, Mollenhauer G, Reinhardt H W

机构信息

Arbeitsgruppe Experimentelle Anästhesie, Universitätsklinikum Rudolf Virchow--Charlottenburg, Freie Universität Berlin, Germany.

出版信息

Am J Physiol. 1995 Sep;269(3 Pt 2):R481-9. doi: 10.1152/ajpregu.1995.269.3.R481.

Abstract

Two groups of six dogs were studied during 4 control days and 4 days of reduced renal perfusion pressure (rRPP) servo controlled at 20% below the individual dog's 24-h mean arterial blood pressure (MABP) during control days, i.e., below the threshold for renin release. On rRPP days, endogenous activation of plasma aldosterone and angiotensin II was inhibited by the angiotensin-converting enzyme inhibitor captopril. The dogs were kept on a high-Na and high-water intake. Unlike studies during rRPP alone, there was no Na and water retention during rRPP+captopril. Glomerular filtration rate dropped by approximately 9%, and MABP remained in the range of control days. Plasma renin activity rose to values 14 times greater than control, whereas plasma aldosterone decreased by approximately 60%. Atrial natriuretic peptide remained in the range of controls. In conclusion, angiotensin-converting enzyme inhibition can prevent the otherwise obligatory Na and water retention and systemic MABP increase during a 20% reduction in renal perfusion pressure. This is achieved most likely via the captopril-induced fall in angiotensin II and plasma aldosterone levels.

摘要

两组各六只狗在4天的对照期和4天肾灌注压降低(rRPP)期接受研究,rRPP期通过伺服控制将肾灌注压维持在低于每只狗对照期24小时平均动脉血压(MABP)的20%,即低于肾素释放阈值。在rRPP期,血管紧张素转换酶抑制剂卡托普利抑制血浆醛固酮和血管紧张素II的内源性激活。狗保持高钠和高水摄入。与单独进行rRPP的研究不同,在rRPP + 卡托普利期间没有钠和水潴留。肾小球滤过率下降约9%,MABP保持在对照期范围内。血浆肾素活性升至比对照高14倍的值,而血浆醛固酮下降约60%。心房利钠肽保持在对照范围内。总之,血管紧张素转换酶抑制可防止肾灌注压降低20%期间出现的必然的钠和水潴留以及全身MABP升高。这很可能是通过卡托普利引起的血管紧张素II和血浆醛固酮水平下降实现的。

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