Isoproterenol infusion increases the maximal tubular capacity of phosphate reabsorption

Isoproterenol, a beta-adrenoreceptor agonist, decreases urinary phosphate (Pi) excretion; however, plasma phosphate concentration also decreases. The purpose of the present study was to determine the effect of isoproterenol infusion on phosphate reabsorption with concomitant phosphate infusions and in the presence and absence of parathyroid hormone (PTH). Clearance experiments were performed on male Sprague-Dawley rats which were acutely thyroparathyroidectomized (TPTX) and successive infusions of phosphate (1, 2, and 3 mumol/min) were used to determine the maximal tubular capacity of phosphate reabsorption (TmPi) factored for the glomerular filtration rate (GFR) in four groups of rats. In the saline-infused control group the TmPi/GFR was 2.87 +/- 0.19 mumol/ml (n = 8). When isoproterenol was infused intravenously at a rate of 0.005 mg/kg/min, urinary cAMP excretion was significantly increased and the TmPi/GFR was 3.53 +/- 0.17 mumol/ml (n = 10, p less than 0.05). In the PTH-infused group (33 U/kg bolus followed by a sustaining infusion of 1 U/kg/min) TmPi/GFR was 1.69 +/- 0.15 mumol/ml (n = 9). Coadministration of isoproterenol and PTH significantly increased the TmPi/GFR to 3.25 +/- 0.64 mumol/ml (n = 9). Basal cAMP excretion was similar in both groups. These results demonstrate that the stimulation of renal beta-adrenoreceptors by isoproterenol infusion markedly increases phosphate reabsorption and reverses the decrease in the maximal tubular capacity of phosphate reabsorption induced by PTH infusion.