Alterations of the renal handling of H+ in diabetic rats

Alterations of the renal handling of H+ in diabetic rats

Author NascimentoGomes, G. Google Scholar
Gil, F. Z. Google Scholar
MelloAires, M. Google Scholar
Institution Universidade Federal de São Paulo (UNIFESP)
Universidade de São Paulo (USP)
Abstract 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.
Keywords diabetes
acid excretion
bicarbonate reabsorption
proximal acidification
Language English
Date 1997-01-01
Published in Kidney & Blood Pressure Research. Basel: Karger, v. 20, n. 4, p. 251-257, 1997.
ISSN 1420-4096 (Sherpa/Romeo, impact factor)
Publisher Karger
Extent 251-257
Access rights Closed access
Type Article
Web of Science ID WOS:A1997YG61300007

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