Attenuation of enhanced tubuloglomerular feedback activity in SHR by renal denervation.
Attenuation of enhanced tubuloglomerular feedback activity in SHR by renal denervation.
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通过去肾神经减弱 SHR 中增强的肾小管肾小球反馈活性。
DOI：
10.1152/ajprenal.1990.258.4.f980
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发表时间：
1990
期刊：
影响因子：
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通讯作者：
N. Hattori
中科院分区：
文献类型：
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作者：
T. Takabatake;Y. Ushiogi;K. Ohta;N. Hattori
在8~10周龄自发性高血压大鼠(SHR)和Wistar-京都大鼠(WKY)上，我们观察了急性单侧肾去神经(DNX)对肾小球反馈(TGF)机制的影响。SHR的平均动脉压(MAP，28%)和肾血管阻力(RVR，35%)较高，而肾血流量(RBF)、肾小球滤过率(GFR)、尿流量和钠排泄相似。DNX不改变MAP，但降低RVR(26%)，增加RBF(29%)、GFR(16%)、尿流量(52%)和钠排出(431%)。DNX对WKY的上述指标无影响。Ringer液Henle循环对SHR早期近端血流速度(EPFR)的影响大于WKY，在20nL/min时有显著差异(9.8+/-0.7vs.6.5+/-0.7nL/min)。DNX使SHR的非灌流EPFR从25.6+/-1.1增加到31.7+/-1.3 nL/min，并降低了20 nL/min(9.8+/-0.7 nL/min对4.4+/-0.7 nL/min)和40 nL/min(14.2+/-1.1 nL/min对10.4+/-0.7 nL/min)的转化生长因子反应。DNX可降低转化生长因子的敏感性，表现为最大反应性降低(-0.89+/-0.14至-0.36+/-0.07)和转折点升高(16.5+/-0.9至25.2+/-2.9nL/min)。DNX不影响WKY的转化生长因子反应。假去神经不改变肾血流动力学和转化生长因子。这些结果表明，肾神经对SHR的肾脏血管和转化生长因子系统有紧张性影响，而对WKY无明显影响。SHR对转化生长因子的反应性增强可能与容量滞留和高血压的维持有关。
We evaluated the effect of acute unilateral renal denervation (DNX) on the tubuloglomerular feedback (TGF) mechanism in Inactin-anesthetized hydropenic male 8- to 10-wk-old spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). SHR had higher mean arterial pressure (MAP, 28%) and renal vascular resistance (RVR, 35%), whereas renal blood flow (RBF), glomerular filtration rate (GFR), urine flow, and sodium excretion were similar. DNX in SHR did not change MAP but decreased RVR (26%) and increased RBF (29%), GFR (16%), urine flow (52%), and sodium excretion (431%). DNX did not affect these in WKY. Loop of Henle perfusion with Ringer solution reduced early proximal flow rate (EPFR) in SHR more than in WKY; significantly different at a loop flow of 20 nl/min (9.8 +/- 0.7 vs. 6.5 +/- 0.7 nl/min). DNX in SHR increased the nonperfused EPFR from 25.6 +/- 1.1 to 31.7 +/- 1.3 nl/min and reduced TGF responses during perfusion at both 20 nl/min (9.8 +/- 0.7 vs. 4.4 +/- 0.7 nl/min) and 40 nl/min (14.2 +/- 1.1 vs. 10.4 +/- 0.7 nl/min). TGF sensitivity was attenuated by DNX, as indicated by reduced maximum reactivity (-0.89 +/- 0.14 to -0.36 +/- 0.07) and increased turning point (16.5 +/- 0.9 to 25.2 +/- 2.9 nl/min). TGF responses in WKY were not influenced by DNX. Sham denervation did not alter renal hemodynamics and TGF. These results indicate that renal nerves exert a tonic influence on the renal vasculature and the TGF system in SHR but not in WKY. Enhanced TGF responsiveness may be involved in volume retention and in the maintenance of hypertension in SHR.