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Acute regulation of parathyroid hormone by dietary phosphate

Renal Division, Washington University School of Medicine, St. Louis, Missouri

Submitted 16 February 2005 ; accepted in final form 18 May 2005

Secondary hyperparathyroidism in chronic renal failure is stimulated by dietary phosphate (P_i) loading and ameliorated by dietary P_i restriction. We investigated the rapidity of the response of serum parathyroid hormone (PTH) to changes in dietary P_i. When uremic rats adapted to a high P_i diet (HPD) were fed a single meal of low P_i diet (LPD), plasma PTH fell 80% within 2 h; plasma P_i fell 1 mg/dl with no change in plasma ionized Ca (ICa). When uremic rats on the HPD were gavaged with LPD, PTH fell 60% within 15 min; plasma P_i fell by 3.0 mg/dl with no change in total plasma Ca. However, HPD gavage increased PTH by 80% within 15 min with no change in plasma P or Ca, suggesting that the response may be independent of altered plasma P_i. Duodenal infusion of sodium P_i increased PTH twofold within 10 min, with no change in ICa but an increase in plasma P_i, whereas duodenal infusion of NaCl had no effect on any of these parameters. Intravenous infusion of sodium phosphate also increased PTH within 10 min with no change in plasma ICa; intravenous NaCl had no effect. Additionally, duodenal infusion of phosphonoformate, a nonabsorbable phosphate analog, increased PTH fourfold within 5 min, but did not change plasma P or ICa. These findings indicate that oral P_i increases PTH release in vivo more rapidly than previously reported; this response may be from both plasma phosphate and an additional signal arising from the gastrointestinal tract.

phosphate; gastrointestinal tract

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