Fernandez R, Malnic G
Department of Physiology and Biophysics, USP, University of São Paulo, Brazil.
J Membr Biol. 1995 Feb;143(3):227-35. doi: 10.1007/BF00233451.
Secretion of bicarbonate has been described for distal nephron epithelium and attributed to apical Cl-/HCO3- exchange in beta-intercalated cells. We investigated the presence of this mechanism in cortical distal tubules by perfusing these segments with acid (pH 6) 10 mM phosphate Ringer. The kinetics of luminal alkalinization was studied in stationary microperfusion experiments by double-barreled pH (ion-exchange resin)/1 M KCl reference microelectrodes. Luminal alkalinization may be due to influx (into the lumen) of HCO3- or OH-, or efflux of H+. The magnitude of the Cl-/HCO3- exchange component was measured by perfusing the lumen with solutions with or without chloride, which was substituted by gluconate. This component was not different from zero in control and alkalotic (chronic plus acute) Wistar rats. Homozygous Brattleboro rats (BRB), genetically devoid of antidiuretic hormone, were used since this hormone has been shown to stimulate H+ secretion, which could mask bicarbonate secretion. In these rats, no evidence for Cl-/HCO3- exchange was found in control BRB and in early distal segments of alkalotic animals, but in late distal tubule a significant component of 0.14 +/- 0.033 nmol/cm2.sec was observed, which, however, is small when compared to the reabsorptive flow found in control Wistar rats, of 0.95 +/- 0.10 nmol/cm2.sec. In addition, 5 x 10(-4) M SITS had no effect on distal bicarbonate reabsorption in controls as well as on secretion in alkalotic Wistar and Brattleboro rats, which is compatible with the absence of effect of this drug on the apical Cl-/HCO3- exchange in other tissues.(ABSTRACT TRUNCATED AT 250 WORDS)
已有研究描述了远端肾单位上皮细胞分泌碳酸氢盐的现象，并将其归因于β - 闰细胞顶端的Cl⁻/HCO₃⁻交换。我们通过用酸性（pH 6）10 mM磷酸盐林格液灌注皮质远端小管节段，研究了该机制在皮质远端小管中的存在情况。在固定微灌注实验中，使用双管pH（离子交换树脂）/1 M KCl参比微电极研究管腔碱化的动力学。管腔碱化可能是由于HCO₃⁻或OH⁻流入（进入管腔），或者H⁺流出所致。通过用含或不含氯离子（用葡萄糖酸盐替代）的溶液灌注管腔来测量Cl⁻/HCO₃⁻交换成分的大小。在对照和碱中毒（慢性加急性）的Wistar大鼠中，该成分与零无差异。使用纯合的Brattleboro大鼠（BRB），其基因上缺乏抗利尿激素，因为已证明该激素会刺激H⁺分泌，这可能掩盖碳酸氢盐分泌。在这些大鼠中，在对照BRB和碱中毒动物的早期远端节段中未发现Cl⁻/HCO₃⁻交换的证据，但在远端小管后期观察到有0.14±0.033 nmol/cm²·秒的显著成分，然而，与对照Wistar大鼠中发现的0.95±0.10 nmol/cm²·秒的重吸收流量相比，该成分较小。此外，5×10⁻⁴ M SITS对对照中的远端碳酸氢盐重吸收以及碱中毒的Wistar和Brattleboro大鼠中的分泌均无影响，这与该药物对其他组织中顶端Cl⁻/HCO₃⁻交换无作用相符。（摘要截断于250字）
