Regulation of renal transport processes and hemodynamics by macrophages and lymphocytes.
Regulation of renal transport processes and hemodynamics by macrophages and lymphocytes.
复制标题
DOI：
10.1152/ajprenal.1990.258.4.f761
复制
发表时间：
1990-04
期刊：
影响因子：
--
通讯作者：
G. Schreiner;D. Kohan
中科院分区：
文献类型：
--
作者：
G. Schreiner;D. Kohan
肾小球和肾小球的炎性疾病的特征在于肾小球血流动力学和肾小管转运过程的许多改变。这些变化背后的细胞机制理论上归因于肾单位毒性和破坏。然而，最近的研究表明，肾脏生理学的许多改变可能是由特异性免疫细胞衍生因子介导的。巨噬细胞在活化时释放多种细胞因子。这些单核因子之一，白细胞介素1，通过直接抑制集合管钠重吸收诱导尿钠排泄。肾小球巨噬细胞释放高度血管收缩化合物，包括白三烯D4和血栓素A2。现在已经证明，在以前不认为具有免疫成分的疾病中，巨噬细胞迁移到肾小体中。急性输尿管梗阻的特征是巨噬细胞和淋巴细胞迅速浸润到肾脏。通过照射清除输尿管梗阻中的免疫细胞浸润，可显著改善肾小球滤过率和肾血流量，并部分纠正钠和水排泄。肾功能的这种免疫调节可能发生在多种肾脏疾病中，其中许多不涉及原发性免疫损伤。我们建议，肾血流动力学和液体和电解质的运输中观察到的状态，其特征在于肾实质细胞之间的免疫细胞共存的异常可能反映了肾细胞生理学的复杂的免疫调节。
Inflammatory diseases of the renal glomerulus and interstitium are characterized by numerous alterations in renal glomerular hemodynamics and tubule transport processes. The cellular mechanisms underlying these changes have been theoretically attributed to nephron toxicity and destruction. However, recent studies suggest that many of the alterations in renal physiology may be mediated by specific immune cell-derived factors. Macrophages release a variety of cytokines on activation. One of these monokines, interleukin 1, induces a natriuresis by direct inhibition of collecting duct sodium reabsorption. Glomerular macrophages release highly vasoconstrictive compounds, including leukotriene D4 and thromboxane A2. Macrophages have now been demonstrated to migrate into the renal interstitium in diseases not previously considered to have an immunological component. Acute ureteral obstruction is characterized by a rapid infiltration of macrophages and lymphocytes into the kidney. Removal of the immune cell infiltrate in ureteral obstruction by irradiation markedly improves glomerular filtration rate and renal blood flow and partially corrects sodium and water excretion. Such immune modulation of renal function is likely to occur in a wide variety of diseases of the kidney, many of which do not involve a primary immunological insult. We propose that the abnormalities in renal hemodynamics and in the transport of fluid and electrolytes observed in states characterized by coexistence of immune cells among renal parenchymal cells may reflect a complex immune modulation of renal cell physiology.