Takenaka T, Forster H, De Micheli A, Epstein M
Nephrology Section, VA Medical Center, Miami, Fla. 33125.
Circ Res. 1992 Aug;71(2):471-80. doi: 10.1161/01.res.71.2.471.
The mechanisms mediating abnormal renal autoregulation in Dahl salt-sensitive (DS) rats have not been fully defined. In the present study, we assessed myogenic responsiveness of interlobular arteries (ILAs), afferent arterioles (AAs), and efferent arterioles in isolated perfused hydronephrotic Dahl rat kidneys. Dahl rats were divided into four groups according to strain (Dahl salt-resistant [DR] or DS rats) and dietary sodium manipulation (rats fed low or high salt diets). Systolic blood pressure was elevated only in DS rats fed the high salt diet (202 +/- 4 mm Hg, p less than 0.05). Myogenic responses were obtained by stepwise elevation of renal arterial pressure. Vessel diameters were determined by computer-assisted videomicroscopy. Preglomerular microvessels of DS and DR rats responded differently to changes in renal arterial pressure. AAs and ILAs manifested diminished myogenic responsiveness to increasing renal arterial pressure in DS rats compared with DR rats (p less than 0.05). Both AAs and ILAs in DS rats manifested a higher threshold pressure for eliciting myogenic responses and a decrease in maximal pressure-induced vasoconstriction. The sensitivity of the AA myogenic response to nifedipine was enhanced in DS rats compared with DR rats (p less than 0.05). For rats fed the high salt diet, preglomerular vessels exhibited reduced myogenic responsiveness in both strains. In contrast to preglomerular microvessels, efferent arterioles from all four groups of rats failed to exhibit pressure-induced vasoconstriction. Our data suggest that diminished myogenic responsiveness of AAs and ILAs in DS rats contributes to impaired renal autoregulation in this strain.
介导 Dahl 盐敏感（DS）大鼠肾脏异常自身调节的机制尚未完全明确。在本研究中，我们评估了分离灌注的肾积水 Dahl 大鼠肾脏中肾小叶间动脉（ILA）、入球小动脉（AA）和出球小动脉的肌源性反应性。根据品系（Dahl 盐抵抗[DR]或 DS 大鼠）和饮食钠控制（喂食低或高盐饮食的大鼠）将 Dahl 大鼠分为四组。仅在喂食高盐饮食的 DS 大鼠中收缩压升高（202±4 mmHg，p<0.05）。通过逐步升高肾动脉压获得肌源性反应。通过计算机辅助视频显微镜测定血管直径。DS 和 DR 大鼠的肾小球前微血管对肾动脉压变化的反应不同。与 DR 大鼠相比，DS 大鼠的 AA 和 ILA 对肾动脉压升高的肌源性反应性降低（p<0.05）。DS 大鼠的 AA 和 ILA 均表现出引发肌源性反应的阈值压力较高，且最大压力诱导的血管收缩减少。与 DR 大鼠相比，DS 大鼠的 AA 肌源性反应对硝苯地平的敏感性增强（p<0.05）。对于喂食高盐饮食的大鼠，两个品系的肾小球前血管均表现出肌源性反应性降低。与肾小球前微血管相反，所有四组大鼠的出球小动脉均未表现出压力诱导的血管收缩。我们的数据表明，DS 大鼠中 AA 和 ILA 的肌源性反应性降低导致该品系肾脏自身调节受损。
