Nitric oxide regulates HCO3- and Na+ transport by a cGMP-mediated mechanism in the kidney proximal tubule.
Nitric oxide regulates HCO3- and Na+ transport by a cGMP-mediated mechanism in the kidney proximal tubule.
复制标题
一氧化氮通过肾近曲小管中 cGMP 介导的机制调节 HCO3- 和 Na 的转运。
DOI：
10.1152/ajprenal.1997.272.2.f242
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发表时间：
1997
期刊：
影响因子：
--
通讯作者：
Tong Wang
中科院分区：
文献类型：
--
作者：
Tong Wang
一氧化氮 (NO) 对血压和肾血流动力学的影响已得到充分证实，但 NO 对肾小管 HCO3- 和 Na+ 转运的影响尚不完全清楚。在本研究中，我们结合肾脏清除和原位微灌注技术来研究NO对大鼠肾脏中Na（FE（Na%））的肾脏排泄以及肾小管吸收液体（J（V））和碳酸氢盐（J（HCO3））的速率的影响。给予一氧化氮合酶抑制剂 N(G)-硝基-L-精氨酸甲酯（L-NAME，6 mg/kg 静脉推注）不会显着改变平均血压和肾小球滤过率。然而，L-NAME 显着增加了尿流率和 FE(Na%)，并且这些效果在 60 分钟内保持不变。添加 L-NAME 显着降低近曲小管中的 J(V) 和 J(HCO3)。相反，添加 1 µM 硝普钠 (SNP) 或 S-亚硝基-N-乙酰青霉胺 (SNAP) 显着增加 J(V) 和 J(HCO3)。当 8-溴鸟苷 3',5'-环单磷酸（8-BrcGMP，1 µM）添加到管腔灌注液中时，也观察到类似的刺激。 SNP和8-BrcGMP对J(V)和J(HCO3)的刺激作用不是相加的。由 SNP 引起的 J(V) 和 J(HCO3) 增加被 Na+/H+ 交换阻断剂乙基异丙基阿米洛利和鸟苷酸环化酶抑制剂亚甲蓝消除。这些结果表明，NO 通过肾近曲小管中的 cGMP 相关途径刺激近曲小管 Na+ 和 HCO3- 转运。
The effects of nitric oxide (NO) on blood pressure and renal hemodynamics are well established, but those of NO on renal tubule HCO3- and Na+ transport are not fully understood. In this study, we combined renal clearance and in situ microperfusion techniques to investigate the effects of NO on the renal excretion of Na (FE(Na%)) and the rates of renal tubule absorption of fluid (J(V)) and bicarbonate (J(HCO3)) in the rat kidney. Administration of the nitric oxide synthase inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME, 6 mg/kg iv bolus) did not change mean blood pressure and glomerular filtration rate significantly. However, L-NAME significantly increased urine flow rate and FE(Na%), and these effects were maintained over a 60-min period. Addition of L-NAME markedly decreased both J(V) and J(HCO3) in the proximal tubule. In contrast, addition of 1 microM sodium nitroprusside (SNP) or S-nitroso-N-acetylpenicillamine (SNAP) significantly increased both J(V) and J(HCO3). Similar stimulation was also observed when 8-bromoguanosine 3',5'-cyclic monophosphate (8-BrcGMP, 1 microM) was added to the luminal perfusate. The stimulatory effects of SNP and 8-BrcGMP on J(V) and J(HCO3) were not additive. The increments in J(V) and J(HCO3) due to SNP were abolished by the Na+/H+ exchange blocker ethylisopropylamiloride and the guanylate cyclase inhibitor methylene blue. These results indicate that NO stimulates proximal tubule Na+ and HCO3- transport through a cGMP-linked pathway in the kidney proximal tubule.