Respiratory alkalosis (RA) is seen in diverse clinical conditions including tissue hypoxia, malignancy, neurologic disorders, febrile states, pregnancy, and hepatic failure. Acute RA causes hypophosphaturia in rats, and this effect on renal phosphate handling is reversed by β-adrenoreceptor antagonism. The objective of the present study was to determine the effect of acute RA on phosphate excretion in human patients in the absence and presence of β-adrenoreceptor antagonism with propranolol. Twelve normal volunteers, 6 women and 6 men, were studied in two phases, once with placebo and once with intravenous infusion of propranolol. In both groups, 30-minute renal clearances were taken during normoventilation (NV) and during acute RA induced by voluntary hyperventilation. Acute RA produced a significant decrease in plasma phosphate (P(Pl)) in the absence (ΔP(Pl) = -0.16 ± 0.03 mmol/L) and the presence (ΔP(Pl) = -0.16 ± 0.05 mmol/L) of propranolol. In the placebo group, fractional excretion of phosphate (FE(Pl)) decreased from 24.1% ± 3.4% in NV to 19.2% ± 2.6% in RA. This was associated with a significant decrease in parathyroid hormone (P(PTH)), from 3.38 ± 0.28 pmol/L in NV to 2.54 ± 0.30 pmol/L in RA. In the propranolol group, FE(Pl) did not change significantly, from 19.1% ± 2.7% in NV to 18.7% ± 3.0% in RA. This also occurred in the face of a decrease in P(PTH), from 4.39 ± 0.53 pmol/L in NV to 2.78 ± 0.33 pmol/L in RA. Thus propranolol selectively changes the response of FE(Pl) to acute RA while leaving the P(Pl) and P(PTH) responses unaltered. This suggests that β-adrenoreceptors play a role in the regulation of the response of renal phosphate handling during acute RA and that this role involves a direct tubular effect on phosphate reabsorption, independent of filtered load and hormonal status. We conclude that β-adrenoreceptor antagonism blunts the hypophosphaturic effect of acute respiratory alkalosis in human subjects.
ASJC Scopus subject areas
- Pathology and Forensic Medicine