Schlatter E, Haxelmans S, Hirsch J, Leipziger J
Westfälische Wilhelms-Universität Münster, Germany.
Pflugers Arch. 1994 Oct;428(5-6):631-40. doi: 10.1007/BF00374587.
The K+ channels of the principal cells of rat cortical collecting duct (CCD) are pH sensitive in excised membranes. K+ secretion is decreased with increased H+ secretion during acidosis. We examined whether the pH sensitivity of these K+ channels is present also in the intact cell and thus could explain the coupling between K+ and H+ secretion. Membrane voltages (Vm), whole-cell conductances (gc), and single-channel currents of K+ channels were recorded from freshly isolated CCD cells or isolated CCD segments with the patch-clamp method. Intracellular pH (pHi) was measured using the pH-sensitive fluorescent dye 2'-7'-bis(carboxyethyl)-5-6-carboxyfluorescein (BCECF). Acetate (20 mmol/l) had no effect on Vm, gc, or the activity of the K+ channels in these cells. Acetate, however, acidified pHi slightly by 0.17 +/- 0.04 pH units (n = 19). Vm depolarized by 12 +/- 3 mV (n = 26) and by 23 +/- 2 mV (n = 66) and gc decreased by 26 +/- 5% (n = 13) and by 55 +/- 5% (n = 12) with 3-5 or 8-10% CO2, respectively. The same CO2 concentrations decreased pHi by 0.49 +/- 0.07 (n = 15) and 0.73 +/- 0.11 pH units (n = 12), respectively. Open probability (Po) of all four K+ channels in the intact rat CCD cells was reversibly inhibited by 8-10% CO2. pHi increased with the addition of 20 mmol/l NH4+/NH3 by a maximum of 0.64 +/- 0.08 pH units (n = 33) and acidified transiently by 0.37 +/- 0.05 pH units (n = 33) upon NH4+/NH3 removal. In the presence of NH4+/NH3 Vm depolarized by 16 +/- 2 mV (n = 66) and gc decreased by 26 +/- 7% (n = 16). The activity of all four K+ channels was also strongly inhibited in the presence of NH4+/NH3. The effect of NH4+/NH3 on Vm and gc was markedly increased when the pH of the NH4+/NH3-containing solution was set to 8.5 or 9.2. From these data we conclude that cellular acidification in rat CCD principal cells down-regulates K+ conductances, thus reduces K+ secretion by direct inhibition of K+ channel activity. This pH dependence is present in all four K+ channels of the rat CCD. The inhibition of K+ channels by NH4+/NH3 is independent of changes in pHi and rather involves an effect of NH3.
大鼠皮质集合管(CCD)主细胞的钾通道在切除的细胞膜中对pH敏感。酸中毒时,随着氢离子分泌增加,钾离子分泌减少。我们研究了这些钾通道的pH敏感性在完整细胞中是否也存在,从而解释钾离子和氢离子分泌之间的偶联关系。采用膜片钳技术,从新鲜分离的CCD细胞或分离的CCD节段记录膜电位(Vm)、全细胞电导(gc)和钾通道的单通道电流。使用pH敏感荧光染料2'-7'-双(羧乙基)-5-6-羧基荧光素(BCECF)测量细胞内pH(pHi)。乙酸盐(20 mmol/L)对这些细胞的Vm、gc或钾通道活性无影响。然而,乙酸盐使pHi轻微酸化0.17±0.04个pH单位(n = 19)。3-5%或8-10%二氧化碳使Vm分别去极化12±3 mV(n = 26)和23±2 mV(n = 66),gc分别降低26±5%(n = 13)和55±5%(n = 12)。相同的二氧化碳浓度分别使pHi降低0.49±0.07(n = 15)和0.73±0.11个pH单位(n = 12)。完整大鼠CCD细胞中所有四种钾通道的开放概率(Po)被8-10%二氧化碳可逆性抑制。加入20 mmol/L NH4+/NH3时,pHi最大增加0.64±0.08个pH单位(n = 33),去除NH4+/NH3后短暂酸化0.37±0.05个pH单位(n = 33)。在存在NH4+/NH3的情况下,Vm去极化16±2 mV(n = 66),gc降低26±7%(n = 16)。在存在NH4+/NH3的情况下,所有四种钾通道的活性也受到强烈抑制。当含NH4+/NH3溶液的pH设定为8.5或9.2时,NH4+/NH3对Vm和gc的影响显著增加。从这些数据我们得出结论,大鼠CCD主细胞中的细胞酸化下调钾电导,从而通过直接抑制钾通道活性减少钾分泌。这种pH依赖性存在于大鼠CCD的所有四种钾通道中。NH4+/NH3对钾通道的抑制与pHi的变化无关,而是涉及NH3的作用。