Identification of a contractile function for renal medullary interstitial cells.
Identification of a contractile function for renal medullary interstitial cells.
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DOI：
10.1172/jci118050
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发表时间：
1995-07
期刊：
影响因子：
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通讯作者：
A. K. Hughes;W. Barry;D. Kohan
中科院分区：
文献类型：
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作者：
A. K. Hughes;W. Barry;D. Kohan
肾髓质间质细胞（RMIC）是肾髓质所特有的。凭借其解剖位置和排列，RMIC 可能会阻碍浓度梯度的轴向消散，从而有助于尿液浓缩。基于对 RMIC 收缩潜力的推测，推测尿浓度具有更积极的作用，但是尚未对 RMIC 收缩进行研究。为了确定这些细胞是否具有收缩性，将培养的大鼠 RMIC 暴露于内皮素-1 (ET-1)（一种与 RMIC 结合的有效血管收缩剂），并使用视频显微镜进行检查。 ET-1（低至 10 pM）导致 RMIC 表面积缓慢发展且呈剂量依赖性减少。 ET-1 显着增加了 F-肌动蛋白微丝染色的数量和强度。硝苯地平不改变 ET-1 诱导的 RMIC 收缩，镍部分减少，H7 完全抑制，表明 ET-1 作用由蛋白激酶 C 介导，部分依赖于受体操作的钙通道。 ET-1 效应不涉及一氧化氮，因为 NG-单甲基-L-精氨酸不会改变 ET-1 诱导的 RMIC 收缩；此外，ET-1对cGMP水平只有很小的影响，对亚硝酸盐的产生没有影响。 PGE2 以自分泌方式抑制 ET 作用，因为吲哚美辛增强了 ET-1 诱导的 RMIC 收缩，而 PGE2 抑制了 ET-1 诱导的 RMIC 收缩。收缩反应并不是 ET-1 独有的，因为加压素还会减少 RMIC 表面积并增加 F-肌动蛋白微丝染色。这些研究表明培养物中的 RMIC 是可收缩的。 RMIC 的收缩可能在改变尿浓度以及调节其他肾髓质功能中发挥作用。
Renomedullary interstitial cells (RMIC) are unique to the renal medulla. By virtue of their anatomic location and arrangement, RMIC may hinder axial dissipation of the concentration gradient, thereby aiding urinary concentration. A more active role in urinary concentration has been postulated on the basis of speculations about RMIC contractile potential, however, RMIC contraction has not been investigated. To determine if these cells are contractile, cultured rat RMIC were exposed to endothelin-1 (ET-1), a potent vasoconstrictor which binds to RMIC, and examined using video microscopy. ET-1 (as low as 10 pM) caused a slowly developing and dose-dependent reduction in RMIC surface area. ET-1 markedly increased the number and intensity of F-actin microfilament staining. ET-1-induced RMIC contraction was not altered by nifedipine, was partially reduced by nickel, and was completely inhibited by H7, indicating that ET-1 action is mediated by protein kinase C and is partially dependent upon receptor-operated calcium channels. The ET-1 effect does not involve nitric oxide since NG-monomethyl-L-arginine did not alter ET-1-induced RMIC contraction; in addition, ET-1 had only a minor effect on cGMP levels and no effect on nitrite production. PGE2 acts in an autocrine manner to dampen ET action since indomethacin potentiates, while PGE2 inhibits, ET-1-induced RMIC contraction. The contractile response is not unique to ET-1 since vasopressin also reduces RMIC surface area and increases F-actin microfiliment staining. These studies demonstrate that RMIC in culture are contractile. The possibility is raised that contraction of RMIC plays a role in modifying urinary concentration as well as regulation of other renal medullary functions.