Proximal tubular HCO3-, H+ and fluid transport during maleate-induced acidification defect
| Autor: | Gerhard Malnic, Nancy Amaral Rebouças, Margarida de Mello-Aires, Maria Monica Elias, Davi Teodoro Fernandes |
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| Rok vydání: | 1984 |
| Předmět: |
Male
medicine.medical_specialty Cell Membrane Permeability Physiology Clinical Biochemistry Lumen (anatomy) Diuresis Biological Transport Active Acid–base homeostasis Membrane Potentials Kidney Tubules Proximal Physiology (medical) Internal medicine medicine Animals Acidosis Acid-Base Equilibrium Chemistry Reabsorption Maleates Acidosis Renal Tubular Membrane transport Hydrogen-Ion Concentration Fluid transport Rats Bicarbonates Endocrinology medicine.symptom Perfusion |
| Zdroj: | Pflugers Archiv : European journal of physiology. 401(3) |
| ISSN: | 0031-6768 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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