Alterations of the renal handling of H+ in diabetic rats

Renal acid excretion and proximal and distal nephron acidification were evaluated 20 days after induction of diabetes, in rats, by intraperitoneal injection of streptozotocin (45 mg/kg). Titratable acidity in urine was measured by microtitration and ammonium excretion (NH4+) by spectrophotometry. Proximal tubular acidification was evaluated by the kinetics of reabsorption of perfused HCO3-. Distal nephron acidification was evaluated by measuring urine - blood pCO(2) differences under alkaline overload. The net acid excretion (titratable acidity + NH4+ - HCO3-) was higher (p < 0.001) in diabetic rates (9.82+/-0.65 mu mol/min/kg, n = 26) than in the control group (6.34+/-0.14, n = 24). Proximal HCO reabsorption was also higher (p<0.001) in diabetic rats (8.38+/-0.11 nmol/cm(2)/s, n=12) than in the control group (2.30+/-0.10, n = 22); however, evaluation of distal nephron H+ secretion by urine-blood pCO(2) methodology was similar in both groups. We concluded that in rats with induced diabetes mellitus there is an increased rate of proximal HCO3- reabsorption, possibly effected by a higher density of Na+/H+ antiporter in the luminal membrane of the proximal tubule and by an increased proton-motive force of the H+ secretory mechanism. The higher rates of H+ secretion generate lower stationary proximal luminal pH and probably maintain the blood pH within the physiological range.