Abstract
In previous studies we have shown stimulation of renal acid excretion in the proximal tubules of rats with diabetes of short duration, with no important alterations in glomerular hemodynamics; on the other hand, in thyroparathyroidectomized rats (TPTX model), a significant decrease in renal acid excretion, glomerular filtration rate (GFR) and renal plasma flow (RPF) was detected. Since important changes in the parathyroid hormone-vitamin D-Ca axis are observed in the diabetic state, the present study was undertaken to investigate the renal repercussions of thyroparathyroidectomy in rats previously made diabetic by streptozotocin (45 mg/kg). Four to 6 days after the induction of diabetes (DM), a group of rats were thyroparathyroidectomized (DM + TPTX). Renal functional parameters were evaluated by measuring the inulin and sodium para-aminohippurate clearance on the tenth day. The decrease in the GFR and RPF observed in TPTX was not reversed by diabetes since the same alterations were observed in DM + TPTX. Net acid (NA) excretion was unchanged in DM (6.19 +/- 0.54), decreased in TPTX (3.76 +/- 0.25) and returned to normal levels in DM + TPTX (5.54 +/- 0.72) when compared to the control group (6.34 +/- 0.14 mumol min-1 kg-1). The results suggest that PTH plays an important vasodilator role regarding glomerular hemodynamics, since in its absence the impairment in GFR and RPF was not reversed by the diabetic state. However, with respect to acid excretion, the presence of diabetes was able to overcome the negative stimulus represented by TPTX.
Highlights
The mechanism of urinary acidification has been shown to be altered in several diseases, as well as in experimental models
In previous studies we have shown stimulation of renal acid excretion in the proximal tubules of rats with diabetes of short duration, with no important alterations in glomerular hemodynamics; on the other hand, in thyroparathyroidectomized rats (TPTX model), a significant decrease in renal acid excretion, glomerular filtration rate (GFR) and renal plasma flow (RPF) was detected
The results suggest that parathyroid hormone (PTH) plays an important vasodilator role regarding glomerular hemodynamics, since in its absence the impairment in GFR and RPF was not reversed by the diabetic state
Summary
The mechanism of urinary acidification has been shown to be altered in several diseases, as well as in experimental models. We showed that an increase in the rate of proximal tubular acidification was demonstrable in rats made diabetic (DM) by intraperitoneal administration of streptozotocin [1] while a significant decrease in this parameter was observed in the thyroparathyroidectomized (TPTX) rat model [2]. Pollock et al [15] showed that parathyroid hormone (PTH) inhibits Na+ and volume reabsorption in the proximal tubule, which could lead to metabolic acidosis, while Bichara et al [16] proposed that hyperparathyroidism could cause metabolic alkalosis of renal origin since the hormone stimulated the tubular excretion of ammonium and titratable acidity
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