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首页> 外文期刊>American Journal of Physiology >Muscarinic activation of Na+-dependent ion transporters and modulation by bicarbonate in rat submandibular gland acinus.
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Muscarinic activation of Na+-dependent ion transporters and modulation by bicarbonate in rat submandibular gland acinus.

机译：毒蕈碱激活Na +依赖性离子转运蛋白并由碳酸氢盐调节大鼠下颌下腺腺泡。

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To investigate the interaction between the ion channels and transporters in the salivary fluid secretion, we measured the membrane voltage (V(m)) and intracellular concentrations of Ca(2+), Na(+) ([Na(+)](c)), Cl(-), and H(+) (pH(i)) in rat submandibular gland acini (RSMGA). After a transient depolarization induced by a short application of acetylcholine (ACh; 5 muM, 20 s), RSMGA showed strong delayed hyperpolarization (V(h,ACh); -95 +/- 1.8 mV) that was abolished by ouabain. In the HCO(3)(-)-free condition, the V(h,ACh) was also blocked by bumetanide, a blocker of Na(+)-K(+)-2Cl(-) cotransporter (NKCC). In the presence of HCO(3)(-) (24 meq, bubbled with 5% CO(2)), however, the V(h,ACh) was not blocked by bumetanide, but it was suppressed by ethylisopropylamiloride (EIPA), a Na(+)/H(+) exchanger (NHE) inhibitor. Similarly, the ACh-induced increase in [Na(+)](c) was totally blocked by bumetanide in the absence of HCO(3)(-), but only by one-half in the presence of HCO(3)(-). ACh induced a prominent acidification of pH(i) in the presence of HCO(3)(-), and the acidification was further increased by EIPA treatment. Without HCO(3)(-), an application of ACh strongly accelerated the NKCC activity that was measured from the decay of pH(i) during the application of NH(4)(+) (20 mM). Notably, the ACh-induced activation of NKCC was largely suppressed in the presence of HCO(3)(-). In summary, the ACh-induced anion secretion in RSMGA is followed by the activation of NKCC and NHE, resulting an increase in [Na(+)](c). The intracellular Na(+)-induced activation of electrogenic Na(+)/K(+)-ATPase causes V(h,ACh). The regulation of NKCC and NHE by ACh is strongly affected by the physiological level of HCO(3)(-).
机译：为了研究唾液分泌物中离子通道和转运蛋白之间的相互作用，我们测量了膜电压（V（m））和细胞内Ca（2 +），Na（+）（[Na（+）]（c ），Cl（-）和H（+）（pH（i））在大鼠下颌腺腺泡（RSMGA）中。经过短暂应用乙酰胆碱（ACh; 5μM，20 s）引起的短暂去极化后，RSMGA显示出强烈的延迟超极化（V（h，ACh）; -95 +/- 1.8 mV），这已被哇巴因所消除。在无HCO（3）（-）的条件下，V（h，ACh）也被布美他尼（Namea +）-K（+）-2Cl（-）辅助转运蛋白（NKCC）的阻滞剂阻滞。然而，在存在HCO（3）（-）（24 meq，用5％CO（2）鼓泡）的情况下，V（h，ACh）未被布美他尼阻滞，但被乙基异丙基丙二酰亚胺（EIPA）抑制， Na（+）/ H（+）交换剂（NHE）抑制剂。同样，在不存在HCO（3）（-）的情况下，布美他尼会完全阻止ACh诱导的[Na（+）]（c）的增加，但在存在HCO（3）（- ）。 ACh在HCO（3）（-）存在下诱导pH（i）显着酸化，并且通过EIPA处理进一步增加了酸化。在没有HCO（3）（-）的情况下，ACh的应用会大大加速NKCC活性，而NKCC活性是从NH（4）（+）（20 mM）的应用过程中pH（i）的下降来衡量的。值得注意的是，在HCO（3）（-）的存在下，ACh诱导的NKCC激活被大大抑制。总之，在RSMGA中ACh诱导的阴离子分泌之后，是NKCC和NHE的活化，导致[Na（+）]（c）的增加。细胞内Na（+）诱导的电原Na（+）/ K（+）-ATPase激活导致V（h，ACh）。 HCh（3）（-）的生理水平强烈影响ACh对NKCC和NHE的调节。

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