van Rodijnen William F, van Lambalgen Ton A, Tangelder Geert-Jan, van Dokkum Richard P E, Provoost Abraham P, ter Wee Piet M
Laboratory for Physiology, Vrije Universiteit Medical Center, Amsterdam, The Netherlands.
Hypertension. 2002 Jan;39(1):111-5. doi: 10.1161/hy1201.096817.
Fawn-Hooded rats possess an increased risk to develop glomerular damage. Both an impaired control of preglomerular resistance and an elevated postglomerular resistance have been implicated. In the present study, we directly assessed the myogenic reactivity of distal interlobular arteries and afferent arterioles from hypertensive and normotensive Fawn-Hooded rats compared with Sprague-Dawley and Wistar rats, which are known to be resistant for developing renal disease. Pressure-response curves were made in isolated perfused hydronephrotic kidneys from these rats. In addition, increasing concentrations of angiotensin II were added to the perfusate to determine the reactivity of interlobular arteries, afferent arterioles, and efferent arterioles to this peptide. Preglomerular vessels from hypertensive and normotensive Fawn-Hooded rats exhibited an impaired reactivity to both pressure and angiotensin II compared with that of Sprague-Dawley and Wistar rats. Basal efferent arteriolar diameters were similar among the 4 strains of rat. In addition, efferent arterioles from hypertensive and normotensive Fawn-Hooded rats displayed a reduced sensitivity to angiotensin II. Our observations demonstrate that in Fawn-Hooded rats, 2 components of preglomerular resistance control are impaired: the myogenic and the angiotensin II response. In addition, efferent arteriolar reactivity to angiotensin II is not elevated but lowered in these rats. Therefore, a deficit in preglomerular resistance control is the most important intrinsic factor involved in the increased susceptibility of Fawn-hooded rats to develop renal disease.
黄褐头大鼠发生肾小球损伤的风险增加。肾小球前阻力控制受损和肾小球后阻力升高都与之有关。在本研究中，我们直接评估了高血压和正常血压的黄褐头大鼠与已知对肾病有抵抗力的斯普拉格-道利大鼠和Wistar大鼠相比，其小叶间动脉和入球小动脉的肌源性反应性。在这些大鼠的离体灌注肾积水肾脏中绘制压力-反应曲线。此外，向灌注液中添加浓度递增的血管紧张素II，以确定小叶间动脉、入球小动脉和出球小动脉对该肽的反应性。与斯普拉格-道利大鼠和Wistar大鼠相比，高血压和正常血压的黄褐头大鼠的肾小球前血管对压力和血管紧张素II的反应性受损。4种品系大鼠的基础出球小动脉直径相似。此外，高血压和正常血压的黄褐头大鼠的出球小动脉对血管紧张素II的敏感性降低。我们的观察结果表明，在黄褐头大鼠中，肾小球前阻力控制的两个组成部分受损：肌源性反应和血管紧张素II反应。此外，这些大鼠的出球小动脉对血管紧张素II的反应性没有升高反而降低。因此，肾小球前阻力控制缺陷是黄褐头大鼠易患肾病的最重要内在因素。
