Effect of dexamethasone on segmental phosphate reabsorption in phosphate-deprived rats.

Abstract

These experiments were designed to test the hypothesis that avid phosphate reabsorption by the pars recta accounts for the resistance to the phosphaturic effects of acute dexamethasone (DEX) and parathyroid hormone (PTH) infusions in rats fed a low-phosphate diet. Acute infusion of DEX [0.4 mg/(kg X h)] increased the fractional delivery of phosphate (FDPi) to the late proximal tubule from 7.1 +/- 2.1 to 14.4 +/- 3.5%, whereas FDPi to the early distal tubule and urine were not different. PTH alone [1 U/(kg X min)] increased FDPi to the late proximal tubule from 4.0 +/- 1.1 to 15.7 +/- 3.7%, whereas FDPi to the early distal tubule or urine was not different. The combination of DEX and PTH further increased FDPi to the late proximal tubule (32.7 +/- 6.4%) and resulted in an increase in fractional excretion of phosphate (FEPi), in spite of the fact that the FDPi to the early distal tubule was not significantly increased. The increased delivered load of phosphate to the pars recta following inhibition of phosphate transport in superficial proximal convoluted tubules resulted in a comparable increase in phosphate reabsorption in the pars recta, based on linear regression analysis, in rats fed low-phosphate diet but not in rats fed normal phosphate diet. These results demonstrate that acute infusion of DEX or PTH inhibits fractional phosphate reabsorption in the superficial proximal tubule but does not result in an increase in FEPi due at least in part to avid phosphate reabsorption in the superficial pars recta in rats fed low-phosphate diet.(ABSTRACT TRUNCATED AT 250 WORDS)