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近髓肾单位入球小动脉血流的自身调节。

Autoregulation of afferent arteriolar blood flow in juxtamedullary nephrons.

作者信息

Takenaka T, Harrison-Bernard L M, Inscho E W, Carmines P K, Navar L G

机构信息

Department of Physiology, Tulane University, School of Medicine, New Orleans, Louisiana 70112.

出版信息

Am J Physiol. 1994 Nov;267(5 Pt 2):F879-87. doi: 10.1152/ajprenal.1994.267.5.F879.

Abstract

Utilizing the in vitro blood-perfused juxtamedullary nephron preparation, we examined the effects of alterations in renal arterial pressure on afferent arteriolar blood flow. With video microscopy and cross-correlation techniques, arteriolar inside diameters and centerline erythrocyte velocity were measured to estimate single afferent arteriolar blood flow. In response to random changes in perfusion pressure, afferent arteriolar diameter (n = 8) varied inversely (-0.53 +/- 0.02%/mmHg), and erythrocyte velocity was directly related (1.4 +/- 0.1%/mmHg). Above 95 mmHg, the slope of the relationship between perfusion pressure and afferent arteriolar blood flow did not differ from zero (0.081 +/- 0.053%/mmHg), suggesting efficient autoregulation. When the tubuloglomerular feedback pathway was interrupted by the addition of furosemide (n = 9) or papillectomy (n = 7), there was attenuation of pressure-induced afferent arteriolar constriction, with impairment in blood flow autoregulation (0.60 +/- 0.05%/mmHg). Superfusion with diltiazem abolished autoregulatory responses in afferent arteriolar diameter and blood flow (1.5 +/- 0.2%/mmHg). These data demonstrate the autoregulation of blood flow of individual afferent arterioles in juxtamedullary nephrons and suggest that both tubuloglomerular feedback-dependent and -independent mechanisms are required for autoregulatory responses.

摘要

利用体外血液灌注的近髓肾单位制备方法,我们研究了肾动脉压力改变对入球小动脉血流量的影响。采用视频显微镜和互相关技术,测量小动脉内径和中心线红细胞速度,以估计单个入球小动脉血流量。针对灌注压力的随机变化,入球小动脉直径(n = 8)呈负相关变化(-0.53±0.02%/mmHg),而红细胞速度呈正相关(1.4±0.1%/mmHg)。在95 mmHg以上,灌注压力与入球小动脉血流量之间关系的斜率与零无差异(0.081±0.053%/mmHg),提示有效的自身调节。当通过添加呋塞米(n = 9)或切除乳头(n = 7)中断肾小管-肾小球反馈途径时,压力诱导的入球小动脉收缩减弱,血流量自身调节受损(0.60±0.05%/mmHg)。用维拉帕米灌注消除了入球小动脉直径和血流量的自身调节反应(1.5±0.2%/mmHg)。这些数据证明了近髓肾单位中单个入球小动脉血流量的自身调节,并表明自身调节反应需要肾小管-肾小球反馈依赖性和非依赖性机制。

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