Isoproterenol increases renal tubular reabsorption of phosphate in X-linked hypophosphatemic (Hyp) mice

Hypophosphatemic (Hyp) mice have a reduced renal retention of phosphate. Th e beta-adrenergic agonist isoproterenol reverses phosphaturia induced by pa rathyroid hormone in the rat. This study determined whether isoproterenol c ould raise the renal tubular maximum transport of phosphate (TmP) in Hyp mi ce. Male 10- to 12-week-old normal and Hyp mice were infused with H-3-inuli n and isoproterenol (0.0, 0.25, 0.5 and 1.0 mu g/kg/min) in 0.9% NaCl. Glom erular filtration rate, plasma phosphate, urinary phosphate excretion, TmP, urinary sodium excretion, and urinary cyclic adenosine monophosphate were measured. As expected, Hyp controls (0.0 dose) had a TmP which was signific antly below that of normal controls: 1.15+/-(SEM) 0.6 (n=9) versus 2.13+/-0 .10 (n=11) mu mol P/ml glomerular filtrate (p<0.001). Isoproterenol at dose s of 0.5 and 1.0 mu g/kg/min elevated the TmP of Hyp mice to the level of n ormal controls: 1.94+/-0.19 (n=7) and 1.98+/-0.10 (n=9) mu mol P/ml glomeru lar filtrate, respectively. These results indicate that the low tubular rea bsorption of phosphate in Hyp mice is not due to a fixed low level of phosp hate transport, but to decreased stimulation of phosphate transporters, sin ce Hyp mouse kidneys increase phosphate reabsorption with suitable stimulus .