Afferent renal nerves exhibit a dual function controlling central sympathetic outflow via afferent electrical activity and influencing intrarenal immunological processes by releasing peptides such as calcitonin-gene-related peptide (CGRP). We tested the hypothesis that increased afferent (ARNA) and efferent renal nerve activity (RSNA) occur with augmented release of CGRP in anti-Thy1.1 nephritis, in which enhanced CGRP release exacerbates inflammation. Nephritis was induced in Sprague-Dawley rats by intravenous injection of OX-7 antibody (1.75 mg/kg), animals were investigated neurophysiologically, electrophysiologically and pathomorphologically six days later. Nephritic rats exhibited proteinuria (169.3±10.2 mg/24 h), with increased RSNA (14.7±0.9 bursts/s vs. control 11.5±0.9 bursts/s; n = 11, P < 0.05). However, ARNA (spikes/s) decreased in nephritis (8.0±1.8 Hz vs. control 27.4±4.1 Hz, n = 11, P < 0.05). In patch-clamp recordings neurons with renal afferents from nephritic rats showed a lower frequency of high activity following electrical stimulation (43.4% vs. 66.4% in controls, P < 0.05). In vitro assays showed that renal tissue from nephritic rats exhibited increased CGRP release via spontaneous (14±3 pg/ml vs. 6.8±2.8 pg/ml in controls; P < 0.05, n = 7) and stimulated mechanisms. In nephritic animals, marked infiltration of macrophages in the interstitium (26±4 cells/mm2) and glomeruli (3.7±0.6 cells/glomerular cross-section) occurred. Pretreatment with the CGRP receptor antagonist CGRP8-37 reduced proteinuria, infiltration and proliferation. In nephritic rats, it can be speculated that afferent renal nerves lose their ability to properly control efferent sympathetic nerve activity while influencing renal inflammation through increased CGRP release.

中文翻译：

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大鼠抗Thy1.1肾炎的肾传入神经支配

肾传入神经表现出双重功能，其通过传入的电活动控制中枢交感神经流出，并通过释放诸如降钙素基因相关肽（CGRP）之类的肽影响肾内免疫过程。我们测试了以下假设：在抗Thy1.1肾炎中，CGRP的释放增加会导致传入（ARNA）和肾神经活动（RSNA）的增加，其中CGRP的释放会加剧炎症。通过静脉注射OX-7抗体（1.75 mg / kg）在Sprague-Dawley大鼠中诱发肾炎，六天后对动物进行了神经生理，电生理和病理形态学检查。肾炎大鼠表现出蛋白尿（169.3±10.2 mg / 24 h），RSNA升高（14.7±0.9突发/ s，对照组11.5±0.9突发/ s； n = 11，P <0.05）。然而，肾炎患者的ARNA（峰值/秒）降低（8.0±1.8 Hz vs.对照组27.4±4.1 Hz，n = 11，P <0.05）。在膜片钳记录中，来自肾病大鼠的肾传入神经元在电刺激后表现出较低的高活动频率（43.4％比对照组的66.4％，P <0.05）。体外试验显示，来自肾病大鼠的肾脏组织通过自发表现出增加的CGRP释放（对照组为14±3 pg / ml，而对照组为6.8±2.8 pg / ml； P <0.05，n = 7）和刺激机制。在肾病动物中，间质（26±4细胞/ mm2）和肾小球（3.7±0.6细胞/肾小球横截面）发生巨噬细胞浸润。用CGRP受体拮抗剂CGRP8-37预处理可减少蛋白尿，浸润和增殖。在肾病大鼠中