Isoproterenol Infusion Increases the Maximal Tubular Capacity of Phosphate Reabsorption

Abstract

Isoproterenol, a β-adrenoreceptor agonist, decreases urinary phosphate (P_i) 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 µmol/min) were used to determine the maximal tubular capacity of phosphate reabsorption (Tm_Pi) factored for the glomerular filtration rate (GFR) in four groups of rats. In the saline-infused control group the Tm_pi/GFR was 2.87 ± 0.19 µmol/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 Tm_Pi/GFR was 3.53 ± 0.17 µmol/ml (n=10, p < 0.05). In the PTH-infused group (33 U/kg bolus followed by a sustaining infusion of 1 U/kg/min) Tm_pi/GFR was 1.69 ± 0.15 µmol/ml (n=9). Coadministration of isoproterenol and PTH significantly increased the Tm_Pi/GFR to 3.25 ± 0.64 µmol/ml (n=9). Basal cAMP excretion was similar in both groups. These results demonstrate that the stimulation of renal β-adrenoreceptors by isoproterenol infusion markedly increases phosphate reabsorption and reverses the decrease in the maximal tubular capacity of phosphate reabsorption induced by PTH infusion.

Isoproterenol Increases Renal Tubular Reabsorption of Phosphate in X-Linked Hypophosphatemic (<i>Hyp</i>) Mice

“…The procedure for this experiment was modified from methods of addition, recent studies in humans [8] and mice [9] with Mü hlbauer et al [4], LeClaire et al [12], and Thornton et al [16]. Eight XLH have found that there are mutations in the PEX treatment groups (four doses ¶two genotypes) were studied with gene, renamed PHEX [10] ( phosphate-regulating gene approximately 10 animals per group.…”

“…Then constant levels of 3 H-inulin (0.09 Ci/h) and isoproterenol of phosphate in male Sprague-Dawley rats [12,13]. -(0.0, 0.25, 0.5, or 1.0 g/kg/min) were infused at 0.6 ml/h throughout Adrenoreceptors responded to -adrenergic agonists and the remainder of the experiment.…”

“…An equilibration period of 40 min followed the first 5 min; then urine was collected for 30 min. Midway antagonists such as isoproterenol and propranolol, rethrough the urine collection period, blood was taken for plasma 3 Hspectively [12,13]. LeClaire et al [12] showed that isoproinulin and phosphate determinations.…”

“…The effects of various doses of isopro-that catecholamines play a role in the regulation of P i reabsorption [18]. terenol on renal phosphate reabsorption, urinary phosphate excretion, and circulating phosphate concentraLeClaire et al [12] reported that infusion of isoproterenol, a -adrenoreceptor agonist, increased phosphate tions were examined. We found that isoproterenol caused a significant rise in renal TmP in both normal and Hyp reabsorption in thyroparathyroidectomized rats as compared with saline-infused rats.…”

Effect of Renal Denervation on Phosphate Excretion in Endotoxemic Rats.

“…In particular, there is no precise information about PTH activity in severe infection. In our previous studies, the renal response to endotoxin (Et) administration was found to be resistant to the phosphaturic effect of PTH [7]; hormonal and blood neutrality alterations, such as an increased norepinephrine excretion, hypocapnia, and metabolic acidosis were observed in these previous studies, and all of these responses inhibit the phosphaturic effect of PTH [9][10][11][12][13][14], in particular the first two factors do it by enhancing renal nerve activity. We, therefore, hypothesized that enhanced renal nerve activity during endotoxemia is responsible for the observed hypophosphaturia.…”