Tuncer M, Vanhoutte P M
Hacettepe University, Faculty of Medicine, Ankara, Turkey.
Blood Press. 1993 Sep;2(3):217-20. doi: 10.3109/08037059309077554.
The possible role of endothelium-derived relaxing factor (EDRF) was investigated in resistance vessels of the kidney obtained from spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats. Kidneys were studied in parallel and perfused with Tyrode's solution at constant optimal flow rates. In the presence of indomethacin, during vasoconstriction (increase in perfusion pressure) produced by prostaglandin F2 alpha, acetylcholine caused a graded dilatation (pressure fall) that was greater in kidneys of WKY than of SHR. Methylene blue and hydroquinone, but not oxyhemoglobin, inhibited the decreases in perfusion pressure induced by acetylcholine, but not those by papaverine. The results suggest that part of the renal vasodilatation induced by acetylcholine is mediated by endothelium-derived relaxing factor, and that the response is impaired in the resistance vessels of the hypertensive rat kidney.
研究了内皮源性舒张因子（EDRF）在自发性高血压大鼠（SHR）和正常血压的Wistar-Kyoto（WKY）大鼠肾脏阻力血管中的可能作用。对肾脏进行平行研究，并以恒定的最佳流速用台氏液灌注。在吲哚美辛存在的情况下，在前列腺素F2α引起的血管收缩（灌注压升高）过程中，乙酰胆碱引起分级舒张（压力下降），WKY大鼠肾脏中的这种舒张大于SHR大鼠。亚甲蓝和对苯二酚可抑制乙酰胆碱诱导的灌注压降低，但不能抑制罂粟碱诱导的灌注压降低。结果表明，乙酰胆碱诱导的肾血管舒张部分是由内皮源性舒张因子介导的，并且在高血压大鼠肾脏的阻力血管中这种反应受损。
