Restoration of phosphaturic response to parathyroid hormone by glucocorticoid treatment in phosphorus-deprived rats.
In phosphate deprivation, the kidney is resistant to the phosphaturic effects of several well-established phosphaturic stimuli, including PTH. We examined whether a low-phosphate diet would render rats unresponsive to the phosphaturic effects of glucocorticoids in the presence and absence of PTH. Treatment with triamcinolone (1 or 50 mg/kg/day) caused phosphaturia in rats fed a low-phosphate diet and also restored rhe phosphaturic effects of PTH. Plasma phosphate was significantly increased with both doses of glucocorticoid. There were no changes in acid-base parameters with the low dose and a compensated metabolic acidosis with the high dose of glucocorticoid. Renal gluconeogenesis was stimulated at both doses and was further enhanced by PTH at the higher dose. We conclude that glucocorticoids reverse the resistance to the phosphaturic phosphate and/or enhanced renal gluconeogenesis.
D000136:Acid-Base Equilibrium / Q000187:drug effects; D000818:Animals; D004032:Diet; D005938:Glucocorticoids / Q000494:pharmacology*; D010281:Parathyroid Hormone / Q000494:pharmacology*; D010710:Phosphates / Q000008:administration & dosage / Q000652:urine*; D051381:Rats; D014221:Triamcinolone / Q000494:pharmacology
D005938:Glucocorticoids; D010281:Parathyroid Hormone; D010710:Phosphates; D014221:Triamcinolone