Neurogenic regulation of renal tubular sodium reabsorption.
Neurogenic regulation of renal tubular sodium reabsorption.
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肾小管钠重吸收的神经源性调节。
DOI：
10.1152/ajprenal.1977.233.2.f73
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发表时间：
1977
期刊：
影响因子：
--
通讯作者：
G. Dibona
中科院分区：
文献类型：
--
作者：
G. Dibona
支持肾小管钠重吸收的直接神经源性控制的作用的证据进行了审查。电子显微镜和荧光组织化学研究表明，肾上腺素能神经末梢与哺乳动物（大鼠、犬和猴）肾小管上皮细胞的基底膜直接接触。肾交感神经的低水平直接或压力感受器反射刺激引起肾小管钠重吸收增加，而不改变肾小球滤过率、肾血流量或肾内血流量分布。通过先前用乙啶或酚苄明治疗肾脏来预防抗利尿。大鼠肾脏微穿刺研究发现近端小管钠重吸收增强。通过使用适当阻断剂的实验，排除了已知在肾神经刺激时从肾脏释放的其他体液因子（血管紧张素II、前列腺素）可能间接介导的抗白尿作用。麻醉的可能影响和不确定性的完整性手术肾去神经和其他管状节段性网站的行动进行了严格的分析。这种机制在病理条件下的钠和水潴留的临床意义进行了讨论，并为今后的工作提出了一个招股说明书。
The evidence supporting a role for direct neurogenic control of renal tubular sodium reabsorption is reviewed. Electron microscopic and fluorescence histochemical studies have demonstrated adrenergic nerve terminals in direct contact with basement membranes of mammalian (rat, dog, and monkey) renal tubular epithelial cells. Low-level direct or baroreceptor reflex stimulation of renal sympathetic nerves produces an increase in renal tubular sodium reabsorption without alterations in glomerular filtration rate, renal blood flow, or intrarenal distribution of blood flow. Antinatriuresis was prevented by prior treatment of the kidney with guanethidine or phenoxybenzamine. Rat kidney micropuncture studies have localized a site of enhanced tubular sodium reabsorption to the proximal tubule. Possible indirect mediation of the antinatriuresis by other humoral agents known to be released from the kidney on renal nerve stimulation (angiotensin II, prostaglandin) was excluded by experiments with appropriate blocking agents. The possible effects of anesthesia and uncertainties about the completeness of surgical renal denervation and other tubular segmental sites of action are critically analyzed. The clinical implications of this mechanism in pathologic conditions of sodium and water retention are discussed and and a prospectus for future work is presented.