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首页> 外文期刊>American Journal of Physiology >Inhibition of bicarbonate reabsorption in the rat proximal tubule by activation of luminal P2Y1 receptors.
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Inhibition of bicarbonate reabsorption in the rat proximal tubule by activation of luminal P2Y1 receptors.

机译：通过激活腔内P2Y1受体抑制大鼠近端小管中的碳酸氢盐重吸收。

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摘要

The present study used a stationary microperfusion technique to investigate in vivo the effect of P2Y1 receptor activation on bicarbonate reabsorption in the rat proximal tubule. Proximal tubules were perfused with a bicarbonate Ringer solution before flow was stopped by means of an oil block. The recovery of lumen pH from the initial value (pH 8.0) to stationary values (pH approximately 6.7) was recorded by a H+-sensitive microelectrode inserted downstream of the perfusion pipette and oil block. The stationary pH value and the t(1/2) of pH recovery were used to calculate bicarbonate reabsorption (JHCO3). Both EIPA and bafilomycin A1 caused significant reductions in proximal tubule JHCO3, consistent with the established contributions of Na/H exchange and H+-ATPase to proximal tubule HCO3 reabsorption. The nucleotides ADP and, to a lesser extent, ATP reduced JHCO3 but AMP and UTP were without effect. 2MeSADP, a highly selective agonist of the P2Y1 receptor, reduced JHCO3 in a dose-dependent manner. MRS-2179, a P2Y1 receptor-specific antagonist, abolished the effect of 2MeSADP, whereas theophylline, an antagonist of adenosine (P1) receptors, did not. The inhibitory action of 2MeSADP was blocked by inhibition of protein kinase C and reduced by inhibition of protein kinase A. The effects of EIPA and 2MeSADP were not additive. The data provide functional evidence for P2Y1 receptors in the apical membrane of the rat proximal tubule: receptor activation impairs acidification in this nephron segment.
机译：本研究使用固定的微灌流技术来研究体内P2Y1受体激活对大鼠近端小管中碳酸氢盐重吸收的影响。用碳酸氢盐林格氏液灌注近端小管，然后通过油塞阻止流动。通过将H +敏感的微电极插入灌注移液器和油块的下游，记录管腔pH从初始值（pH 8.0）恢复到固定值（pH约6.7）。固定的pH值和pH回复的t（1/2）用于计算碳酸氢盐的重吸收（JHCO3）。 EIPA和bafilomycin A1均导致近端小管JHCO3的显着减少，这与Na / H交换和H + -ATPase对近端小管HCO3重吸收的确定贡献一致。核苷酸ADP和ATP在较小程度上还原了JHCO3，但AMP和UTP没有作用。 2MeSADP是P2Y1受体的高度选择性激动剂，它以剂量依赖性方式减少JHCO3。 MRS-2179，一种P2Y1受体特异性拮抗剂，取消了2MeSADP的作用，而茶碱，一种腺苷（P1）受体的拮抗剂，则没有。 2MeSADP的抑制作用被蛋白激酶C的抑制所阻断，而被蛋白激酶A的抑制所减弱。EIPA和2MeSADP的作用不是累加的。数据为大鼠近端小管的顶膜中的P2Y1受体提供了功能性证​​据：受体激活削弱了该肾单位段的酸化。

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