Pressure-dependent contraction of rat juxtamedullary afferent arterioles.
Pressure-dependent contraction of rat juxtamedullary afferent arterioles.
复制标题
大鼠近髓传入小动脉的压力依赖性收缩。
DOI：
10.1161/01.res.64.4.790
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发表时间：
1989
影响因子：
20.1
通讯作者：
Harder,DR
中科院分区：
文献类型：
--
作者：
Sanchez-Ferrer,CF;Roman,RJ;Harder,DR
在大鼠传入小动脉中，用分离的髓旁肾元制备液灌注含有5%白蛋白的生理盐水，研究了压力-直径关系。血管紧张素I（10微米）、血管紧张素II（0.1微米）和去甲肾上腺素（10微米）增加灌注压，去甲肾上腺素收缩传入小动脉，而血管紧张素I或II没有收缩，表明血管反应性强。在灌注压力为80 mm Hg时，表现出压力依赖性收缩的传入小动脉（n = 58）的对照直径平均为30.8 +/- 1.1微米，当灌注压力从80增加到120，再增加到180 mm Hg时，这些小动脉直径减少16.4 +/- 2.1%。在80、120和180 mm Hg的灌注压力下，肾小球毛细血管压力自动调节良好，平均分别为45.2 +/- 2.2、50.2 +/- 2.4和53.0 +/- 3.0 mm Hg。使用血管扩张剂或无Ca2+溶液消除压力升高时的收缩反应；相反，当压力从80毫米汞柱增加到180毫米汞柱时，这些血管的直径分别显著增加17.5 +/- 5.1%和32.0 +/- 9.4%。阻断小管肾小球反馈机制，用速尿或通过去除肾乳头（它会中断液体向致密斑的输送），消除了传入小动脉的压力依赖性收缩。当压力从80 mm Hg增加到120 mm Hg，再增加到180 mm Hg时，这些血管的直径分别增加了27.0 +/- 7.8%和36.0 +/- 5.6%。这些结果表明，体外灌注的髓旁肾单位可以自动调节肾小球毛细血管压力。（摘要删节250字）
Pressure-diameter relations were studied in rat afferent arterioles using an isolated, juxtamedullary nephron preparation perfused with a saline solution containing 5% albumin. Angiotensin I (10 microM), angiotensin II (0.1 microM), and norepinephrine (10 microM) increased perfusion pressure, and norepinephrine, but not angiotensin I or II, contracted afferent arterioles, indicating that the vessels are reactive. The control diameter of the afferent arterioles that exhibited pressure-dependent contraction (n = 58) averaged 30.8 +/- 1.1 micron at perfusion pressure of 80 mm Hg. When pressure was increased from 80 to 120 and then to 180 mm Hg, the diameter of these arterioles decreased by 16.4 +/- 2.1%. Glomerular capillary pressure was well autoregulated and averaged 45.2 +/- 2.2, 50.2 +/- 2.4, and 53.0 +/- 3.0 mm Hg, respectively, at perfusion pressures of 80, 120, and 180 mm Hg. Administration of vasodilators or a Ca2+-free solution eliminated the contractile response to pressure elevations; rather, the diameter of these vessels increased significantly by 17.5 +/- 5.1% and 32.0 +/- 9.4%, respectively, when pressure was increased from 80 to 180 mm Hg. Blocking tubuloglomerular feedback mechanism, with furosemide or by removal of the renal papilla (which interrupts the delivery of fluid to the macula densa), eliminated the pressure-dependent contraction of the afferent arterioles. Instead the diameter of these vessels increased by 27.0 +/- 7.8% and 36.0 +/- 5.6%, respectively, when the pressure was increased from 80 to 120 and then to 180 mm Hg. These results demonstrate that juxtamedullary nephrons perfused in vitro autoregulate glomerular capillary pressure.(ABSTRACT TRUNCATED AT 250 WORDS)