Esquerro E, Rivas-Cabãnero L, López-Novoa J M
Departamento de Fisiologia y Farmacologia Facultad de Medicina Universidad de Salamanca, Spain.
Ren Fail. 1995 Nov;17(6):689-94. doi: 10.3109/08860229509037636.
We evaluated the properties of glomerular angiotensin II receptors in renal glomeruli isolated from control rats and from rats with gentamicin-induced renal failure. There were no differences in the affinity of angiotensin II for its receptor between glomeruli from control and those from rats treated with gentamicin. Angiotensin II receptor density was lower in glomeruli from rats with renal failure than in those from control rats (985 +/- 71 in gentamicin treated rats vs. 1602 +/- 213 fmol/mg prot in controls). No significant differences were observed in renin activity in the supernatant from glomeruli isolated from control rats (3.74 +/- 0.29 ng angiotensin l/mL h) and those isolated from rats with gentamicin-induced renal failure (2.99 +/- 0.29 ng angiotensin l/mL h, p > 0.1). These findings do not support the contention of a role of angiotensin II in the development and maintenance of gentamicin-induced ARF.
我们评估了从对照大鼠和庆大霉素诱导的肾衰竭大鼠分离出的肾肾小球中肾小球血管紧张素II受体的特性。对照大鼠肾小球与庆大霉素处理大鼠肾小球中血管紧张素II与其受体的亲和力没有差异。肾衰竭大鼠肾小球中的血管紧张素II受体密度低于对照大鼠(庆大霉素处理大鼠为985±71,对照大鼠为1602±213 fmol/mg蛋白)。从对照大鼠分离的肾小球上清液中的肾素活性(3.74±0.29 ng血管紧张素I/mL·h)与从庆大霉素诱导的肾衰竭大鼠分离的肾小球上清液中的肾素活性(2.99±0.29 ng血管紧张素I/mL·h,p>0.1)之间未观察到显著差异。这些发现不支持血管紧张素II在庆大霉素诱导的急性肾衰竭的发生和维持中起作用的观点。