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集合管细胞中调节性容积增加的机制。

Mechanisms of regulatory volume increase in collecting duct cells.

作者信息

Fu W J, Kuwahara M, Cragoe E J, Marumo F

机构信息

Second Department of Internal Medicine, Tokyo Medical and Dental University, Japan.

出版信息

Jpn J Physiol. 1993;43(6):745-57. doi: 10.2170/jjphysiol.43.745.

DOI:10.2170/jjphysiol.43.745
PMID:8007444
Abstract

To examine the mechanisms of cell volume regulation in response to hyperosmolality, segments of the inner stripe of rabbit outer medullary collecting duct (OMCDi) were perfused in vitro. The cross-sectional area of the tubule was monitored as an index of the relative cell volume. When luminal and basolateral osmolalities were increased from 290 to 390 mOsm simultaneously, the tubule cell shrank instantaneously and reswelled gradually, showing the so-called regulatory volume increase (RVI). Basolateral Na+ removal and addition of basolateral ethyl isopropyl amiloride (EIPA) decreased the RVI response by 76 and 66%, respectively. By contrast, apical Na+ removal had no effect on this response. RVI response was also inhibited by basolateral, but not luminal, Cl- removal (-63%), by total HCO3- removal (-74%), and by adding basolateral 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS) (-62%). Intracellular pH did not change significantly during RVI. Vasopressin increased RVI response by 56%. However, this increase was abolished in the absence of basolateral Na+ and Cl-, and in the presence of basolateral EIPA and DIDS. These results suggest that major mechanisms responsible for RVI are Na(+)-H+ and Cl(-)-HCO3- exchange systems in the basolateral membrane, and that these systems are stimulated by vasopressin in rabbit OMCDi.

摘要

为研究细胞在高渗状态下体积调节的机制,对兔外髓集合管内带(OMCDi)节段进行了体外灌注。监测小管的横截面积作为相对细胞体积的指标。当管腔和基底外侧渗透压同时从290 mOsm升高到390 mOsm时,小管细胞立即收缩并逐渐再膨胀,表现出所谓的调节性容积增加(RVI)。去除基底外侧Na⁺以及添加基底外侧乙基异丙基氨氯地平(EIPA)分别使RVI反应降低了76%和66%。相比之下,去除顶端Na⁺对该反应无影响。去除基底外侧而非管腔Cl⁻(-63%)、去除总HCO₃⁻(-74%)以及添加基底外侧4,4'-二异硫氰基芪-2,2'-二磺酸(DIDS)(-62%)也可抑制RVI反应。在RVI过程中细胞内pH没有显著变化。血管加压素使RVI反应增加了56%。然而,在没有基底外侧Na⁺和Cl⁻以及存在基底外侧EIPA和DIDS的情况下,这种增加被消除。这些结果表明,负责RVI的主要机制是基底外侧膜中的Na⁺-H⁺和Cl⁻-HCO₃⁻交换系统,并且这些系统在兔OMCDi中受到血管加压素的刺激。

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