Veron D, Martin R S, Escobar E, Tufaro D, Visconti P, Tezon J G, Arrizurieta E E
Instituto de Investigaciones Médicas Alfredo Lanari, University of Buenos Aires, Argentina.
Acta Physiol Scand. 1994 May;151(1):45-50. doi: 10.1111/j.1748-1716.1994.tb09719.x.
Secondary hyperaldosteronism enhances the rate of K secretion in distal colon, at least in part, through the stimulation of Na(+)-K(+)-Cl- cotransport across the basolateral membrane. To maintain a constant intracellular Cl- activity an increase in Cl- transport out of the cell must be assumed. We explored, under amiloride 10(-4) M and short circuited conditions, conductive pathways for Cl- exit in the distal colon of K(+)-adapted rats by means of a putative Cl- channel blocker, NPPB (5-nitro-2(3-phenyl-propylamino-benzoate. Results prior to NPPB showed an increase in JClms after K+ loading from 5.84 +/- 0.66 to 8.33 +/- 0.86 and JClsm from 4.77 +/- 0.55 to 8.16 +/- 0.96 microEq h-1 cm-2 (P < 0.001), when compared with controls. Net fluxes were not different between groups. Luminal NPPB in K+ adaptation resulted in a decrease of JClsm, from 7.85 +/- 1.5 to 6.69 +/- 1.5 microEq h-1 cm-2 (P < 0.05). There were no changes in both unidirectional Cl- fluxes in controls under luminal NPPB and in potential difference (V) and short-circuit current (Isc) under any condition. Finally, K+ adaptation resulted in an increase of luminal cyclic AMP (cAMP) concentration (0.09 +/- 0.02 to 0.20 +/- 0.03 pmol 100 microliters -1, P < 0.005), when compared with control rats. The data may suggest a transcellular recycling of Cl- and an activated NPPB inhibitable serosal to mucosal Cl- pathway on luminal membrane in the K+ adapted state, possibly mediated by an increase in cAMP production.
继发性醛固酮增多症至少部分通过刺激钠钾氯共转运体跨基底外侧膜转运，提高了远端结肠的钾分泌速率。为维持细胞内氯离子活性恒定，必然存在氯离子转运出细胞的增加。我们在10⁻⁴M氨氯吡咪和短路条件下，使用一种假定的氯离子通道阻滞剂NPPB（5-硝基-2（3-苯基丙基氨基）苯甲酸酯），探究钾适应大鼠远端结肠中氯离子流出的传导途径。在给予NPPB之前的结果显示，与对照组相比，钾负荷后氯离子跨黏膜短路电流（JClms）从5.84±0.66增加到8.33±0.86，氯离子跨黏膜电流（JClsm）从4.77±0.55增加到8.16±0.96微当量·小时⁻¹·厘米⁻²（P<0.001）。各组间净通量无差异。钾适应状态下管腔内给予NPPB导致JClsm从7.85±1.5降低到6.69±1.5微当量·小时⁻¹·厘米⁻²（P<0.05）。管腔内给予NPPB时，对照组的单向氯离子通量以及任何条件下的电位差（V）和短路电流（Isc）均无变化。最后，与对照大鼠相比，钾适应导致管腔内环磷酸腺苷（cAMP）浓度升高（从0.09±0.02升高到0.20±0.03皮摩尔/100微升，P<0.005）。这些数据可能提示在钾适应状态下，氯离子存在跨细胞循环，且在管腔膜上存在一种可被NPPB抑制的从浆膜到黏膜的氯离子途径，可能由cAMP生成增加介导。
