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致密斑控制肾素分泌的机制。

The macula densa mechanism for control of renin secretion.

作者信息

Lorenz J N, Greenberg S G, Briggs J P

机构信息

Department of Physiology, University of Michigan, Ann Arbor.

出版信息

Semin Nephrol. 1993 Nov;13(6):531-42.

PMID:8278686
Abstract

Many questions remain concerning the precise mechanism by which the luminal signal for renin secretion is transmitted from the MD to the JG granular cell. It appears likely that a number of pathways may participate in MD-mediated changes in renin release, some of the agents serving to modulate release, others participating directly in signal transmission. Collectively, the current information suggests a transmission pathway that involves several steps. First, changes occurring in MD NaCl transport, which result directly from alterations in luminal NaCl concentration, act to initiate the response. Second, conveyance of this signal to the extraglomerular mesangial cells via a change in the ionic environment of the EGM field and/or a paracrine factor produced by the MD (perhaps NO) appear likely to be the next step. The subsequent steps probably include changes in prostaglandin production by the EGM, and possible participation of other paracrine factors produced by both endothelial and extraglomerular mesangial cells.

摘要

关于肾素分泌的管腔信号从致密斑(MD)传递至球旁(JG)颗粒细胞的确切机制,仍存在许多问题。似乎有多种途径可能参与致密斑介导的肾素释放变化,其中一些因子用于调节释放,另一些则直接参与信号传递。总体而言,目前的信息提示了一条涉及多个步骤的传递途径。首先,管腔氯化钠浓度改变直接导致的致密斑氯化钠转运变化,起到启动反应的作用。其次,通过肾小球系膜外(EGM)区域离子环境的改变和/或致密斑产生的旁分泌因子(可能是一氧化氮)将该信号传递至肾小球系膜外细胞,似乎是下一步。后续步骤可能包括肾小球系膜外细胞前列腺素生成的变化,以及内皮细胞和肾小球系膜外细胞产生的其他旁分泌因子可能的参与。

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