环孢素诱导的大鼠高血压中肾素-血管紧张素系统各成分的血管收缩反应。

Vasoconstrictor responses to components of the renin-angiotensin system in cyclosporin-induced hypertension in the rat.

Rolls K A, Phillips P A, Aldred K, Hardy K J

Department of Medicine, University of Melbourne, Austin Hospital, Heidelberg, Victoria, Australia.

Clin Exp Pharmacol Physiol. 1994 Mar;21(3):227-30. doi: 10.1111/j.1440-1681.1994.tb02502.x.

Abstract

Since plasma renin activity is increased in cyclosporin A (CsA)-induced hypertension in the rat, the role of the vascular renin-angiotensin system (RAS) in CsA-induced hypertension was investigated in rat mesenteric resistance vessels. 2. Female Wistar rats received CsA (10 mg/kg per day, s.c.) or vehicle for 30 days. CsA treatment increased tail-cuff systolic blood pressure (CsA treated 135 +/- 3 mmHg vs control 125 +/- 1 mmHg, P < 0.0001). 3. Mesenteric resistance arteries (200-300 microns) were isolated and mounted in a microvessel myograph. Concentration-response curves to tetradecapeptide renin substrate (10(-11)-10(-6) mol/L), angiotensin I (10(-11)-10(-6) mol/L) and angiotensin II (10(-12)-10(-6) mol/L) showed no differences between CsA-treated and control groups. 4. Mesenteric vascular angiotensin-converting enzyme (ACE) characteristics were determined by radioligand binding. There were no differences in the content or affinity of ACE between CsA-treated and control rats. 5. These results suggest that the mesenteric vascular RAS does not play a major role in CsA-induced hypertension in the rat.

摘要

由于环孢素A（CsA）诱导的大鼠高血压中血浆肾素活性升高，因此在大鼠肠系膜阻力血管中研究了血管肾素-血管紧张素系统（RAS）在CsA诱导的高血压中的作用。2. 雌性Wistar大鼠接受CsA（每天10mg/kg，皮下注射）或赋形剂，持续30天。CsA治疗可提高尾袖收缩压（CsA治疗组为135±3mmHg，对照组为125±1mmHg，P<0.0001）。3. 分离肠系膜阻力动脉（200-300微米）并安装在微血管肌动描记器中。对十四肽肾素底物（10^(-11)-10^(-6)mol/L）、血管紧张素I（10^(-11)-10^(-6)mol/L）和血管紧张素II（10^(-12)-10^(-6)mol/L）的浓度-反应曲线在CsA治疗组和对照组之间没有差异。4. 通过放射性配体结合测定肠系膜血管血管紧张素转换酶（ACE）特性。CsA治疗组和对照组大鼠之间ACE的含量或亲和力没有差异。5. 这些结果表明，肠系膜血管RAS在CsA诱导的大鼠高血压中不发挥主要作用。