Rebouças N A, Fernandes D T, Elias M M, de Mello-Aires M, Malnic G
Pflugers Arch. 1984 Jul;401(3):266-71. doi: 10.1007/BF00582594.
The mechanism of tubular acidification was studied in proximal tubular acidification defect induced in rats by acute parenteral infusion of maleate (200 mg/kg), which causes diuresis and bicarbonaturia. Proximal tubular bicarbonate reabsorption and H+ ion secretion were determined by stopped-flow microperfusion and measurement of luminal pH by Sb microelectrodes. Stationary pH increased in proximal tubule from 6.78 to 7.25 and bicarbonate reabsorption decreased from 1.32 to 0.51 nmol/cm2 X s. In these segments, mean cell PD fell from -66.6 to -20.2 mV, while Jv as estimated by the Gertz technique fell to 15% of controls. A similar impairment of acidification was observed during luminal and capillary perfusion with phosphate Ringer's. Since H+-ion efflux from the lumen was not significantly increased and both acidification and alkalinization half-times (t/2) were increased, no evidence for an increase in passive permeability for H+/HCO3- was obtained. The increased t/2 found during luminal perfusion with acid phosphate indicates, according to an electrical analog model, a reduction in pump series conductance. These results show that maleate affects both proximal Na+ and H+ transport; this effect may be ascribed to impairment of sodium-dependent transport systems in the brush-border membrane.
通过急性非肠道输注马来酸盐（200mg/kg）诱导大鼠近端肾小管酸化缺陷，研究肾小管酸化机制，该输注可导致利尿和重碳酸盐尿。通过停流微灌注以及用锑微电极测量管腔pH值来测定近端肾小管重碳酸盐重吸收和H⁺离子分泌。近端小管的稳态pH值从6.78升至7.25，重碳酸盐重吸收从1.32降至0.51nmol/cm²·s。在这些节段中，平均细胞电位差从-66.6mV降至-20.2mV，而通过格茨技术估算的Jv降至对照组的15%。在用磷酸盐林格液进行管腔和毛细血管灌注时观察到类似的酸化受损情况。由于管腔中H⁺离子外流未显著增加，且酸化和碱化半衰期（t/2）均增加，未获得H⁺/HCO₃⁻被动通透性增加的证据。根据电模拟模型，在用酸性磷酸盐进行管腔灌注时发现t/2增加表明泵串联电导降低。这些结果表明马来酸盐影响近端Na⁺和H⁺转运；这种作用可能归因于刷状缘膜中钠依赖性转运系统的损伤。
