Medeiros I A, Zhang B L, Bertolino S, Sassard J
Département de Physiologie et Pharmacologie Clinique, URA CNRS 1483, Faculté de Pharmacie, Lyon, France.
J Hypertens. 1994 Aug;12(8):871-7.
To assess whether the pressure-independence of renin release by isolated kidneys of Lyon hypertensive (LH) rats could result from long-term exposure to high blood pressure, sodium retention or an altered regulation of intracellular calcium through L-type voltage operated channels.
Renin release was studied in kidneys from LH rats, either controls or chronically (aged 3-7 weeks) treated with hydralazine or deprived of sodium. The influence of L-type calcium channels was studied acutely using a specific activator (BAY K8644) or modulator (verapamil). Lyon low blood pressure (LL) rats served as controls.
Kidneys were isolated from LH or LL rats aged 7 weeks and single-pass perfused at three pressure levels: 70, 85 and 160 mmHg.
LH rat kidneys differed from LL rat kidneys in having elevated vascular resistances, decreased glomerular filtration rate, pressure natriuresis and pressure-dependent renin release. Hydralazine treatment and sodium deprivation did not significantly modify the pressure-independence of renin release by LH rat kidneys. BAY K8644 (1 x 10(-8) and 5 x 10(-8) mol/l) induced significantly greater vasoconstrictor effects in LH than in LL rat kidneys but did not affect the renin release already stimulated by low perfusion pressure. Verapamil (5 x 10(-6) mol/l) dilated LH more than LL rat kidneys. It did not change the renin release observed at low, but enhanced it at high, perfusion pressure. This effect was more marked in LL than in LH rat kidneys.
The poor stimulation of renin release by low perfusion pressure in LH rat kidneys does not appear to be a consequence of high blood pressure level, sodium retention and alteration in L-type calcium channels. However, results demonstrate that these channels participate in the increased vascular resistances exhibited by LH rat kidneys.
评估里昂高血压（LH）大鼠离体肾脏肾素释放的压力独立性是否源于长期暴露于高血压、钠潴留或通过L型电压门控通道对细胞内钙调节的改变。
研究LH大鼠肾脏的肾素释放情况，将其分为对照组、用肼屈嗪进行长期（3 - 7周龄）治疗组或钠缺乏组。使用特异性激活剂（BAY K8644）或调节剂（维拉帕米）急性研究L型钙通道的影响。里昂低血压（LL）大鼠作为对照。
从7周龄的LH或LL大鼠分离肾脏，并在三个压力水平：70、85和160 mmHg下进行单通道灌注。
LH大鼠肾脏与LL大鼠肾脏的不同之处在于血管阻力升高、肾小球滤过率降低、压力性钠排泄和压力依赖性肾素释放。肼屈嗪治疗和钠缺乏并未显著改变LH大鼠肾脏肾素释放的压力独立性。BAY K8644（1×10⁻⁸和5×10⁻⁸ mol/l）在LH大鼠肾脏中诱导的血管收缩作用明显大于LL大鼠肾脏，但不影响低灌注压力已刺激的肾素释放。维拉帕米（5×10⁻⁶ mol/l）使LH大鼠肾脏的扩张程度大于LL大鼠肾脏。它在低灌注压力下未改变观察到的肾素释放，但在高灌注压力下增强了肾素释放。这种作用在LL大鼠肾脏中比在LH大鼠肾脏中更明显。
LH大鼠肾脏中低灌注压力对肾素释放的刺激不足似乎不是高血压水平、钠潴留和L型钙通道改变的结果。然而，结果表明这些通道参与了LH大鼠肾脏表现出的血管阻力增加。
