The Sodium-Bicarbonate Cotransporter 1 (NBC1) and Monocarboxylate Transporter 1 (MCT1) in the Rat Kidney are Regulated in Response to Metabolic Acidosis

The present work was designed to study the effect of metabolic acidosis induced by ammonium chloride on the expression of sodium-bicarbonate cotransporter 1 (NBC1) and Monocarboxylate transporter 1 (MCT1) in rat kidney. Following the treatment of NH4Cl, blood pH and bicarbonate concentration were significantly decreased, while significant increase in chloride concentration was developed. Moreover, urine analysis revealed decrease in urine pH and significant increase in ammonia in acidotic rats. The protein expression of NBC1 and MCT1 was determined in the rat kidney by immunofluorescence confocal laser-scanning microscopy and Western blotting analyses. In the experimental group, the expression level of NBC1 was significantly increased in the renal proximal tubules, whereas, the expression of MCT1 was significantly decreased. Western blotting data confirmed the immunofluorescence confocal laser-scanning microscopy. In conclusion, metabolic acidosis causes adaptive increases in the basolateral NBC1 in the rat renal proximal tubule that are likely responsible for the increased ability of the proximal tubule to reabsorb filtered bicarbonates. Additionally, acidosis leads to decrease the MCT1 protein expression level in renal proximal tubule that may explain the increase in lactate excretion in the urine of acidotic rats due to the reduction in lactate co-transport.