Control of proximal tubule acidification by the endothelium of the peritubular capillaries.
Control of proximal tubule acidification by the endothelium of the peritubular capillaries.
复制标题
通过管周毛细血管内皮控制近端小管酸化。
DOI：
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发表时间：
1997
影响因子：
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通讯作者：
Ariel F. Castro
中科院分区：
文献类型：
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作者：
C. Amorena;Ariel F. Castro
鸟苷3 '，5'-环一磷酸（cGMP）是一种一氧化氮介体，可刺激肾皮质刷状缘囊泡中的Na+/H+交换。本工作的目的是测试是否肾小管周围毛细血管的内皮调制近端管腔酸化的速度通过释放内皮源性一氧化氮（EDNO）。用二丁酰cGMP灌注小管腔增加了净质子通量（J（H））。两种引起EDNO产生的药物，缓激肽（BK）和氨甲酰胆碱（Cch），当加入到肾小管周围毛细血管灌注液中时，增加了J（H）。用无钠溶液灌流肾小管周围毛细血管和管腔时，缓激肽对J（H）无影响。亚甲蓝（MB）和N（G）-硝基-L-精氨酸甲酯（L-NAME）可阻断Cch引起的J（H）升高，并降低基础J（H）。缓激肽增加cGMP含量的孤立近曲小管，但只有当他们与内皮细胞共孵育。BK的这种作用可被L-NAME阻断。结果提示，肾小管周毛细血管内皮细胞通过改变近曲小管细胞cGMP水平影响近曲小管酸化，可能是通过刺激Na ~+/H ~+交换器。
Guanosine 3',5'-cyclic monophosphate (cGMP), a nitric oxide mediator, stimulates Na+/H+ exchange in brush-border vesicles of the renal cortex. The aim of the present work was to test whether the endothelium of the peritubular capillaries modulated the rate of proximal luminal acidification through the release of endothelium-derived nitric oxide (EDNO). Perfusion of the tubule lumen with dibutyryl cGMP increased net proton flux (J(H)). Two agents that elicit EDNO production, bradykinin (BK) and carbamylcholine (Cch), increased J(H) when added to the peritubular capillary perfusate. Bradykinin did not affect J(H) when the peritubular capillaries and the lumen were perfused with Na-free solution. Methylene blue (MB) and N(G)-nitro-L-arginine methyl ester (L-NAME) blocked the elevation in J(H) by Cch and also decreased basal J(H). Bradykinin increased cGMP content of isolated proximal convoluted tubules, but only if they were coincubated with endothelial cells. This effect of BK was blocked by L-NAME. The results suggest that the endothelium of the peritubular capillaries affects proximal tubule acidification through changes of cGMP in proximal tubule cells, probably via stimulation of Na+/H+ exchanger.