Effect of parathyroid hormone on renal excretion of sodium and hydrogen ions
The contribution of parathyroid hormone (PTH) to the renal adjustment of phosphate transport has been extensively investigated, whereas the action of this hormone on bicarbonate and hydrogen excretion has not received as much attention.Nineteen dogs were studied before and during a 2-h infusion of PTH in the left renal artery (8 mU/min per kilogram) under slight expansion of extracellular volume (fractional sodium excretion = U/FNa = 3.8 ± 0.3%). Group I (n = 7) was studied under normal acid–base condition while group II (n = 6) was studied during metabolic acidosis. Bicarbonate titration curves were obtained from group III (n = 6) in which the right kidney was used as control. In all studies, plasma pCO2 was kept constant.[Formula: see text] rose from 4.2 ± 1.1 to 15.6 ± 3.0% and from 3.8 ± 0.4 to 25.0 ± 3.5% in groups I and II, respectively. U/FNa was unchanged in both groups. [Formula: see text] rose from 5.8 ± 0.6 to 10.1 ± 0.7% in group I but remained at 1.0 ± 0.2% in group II during PTH. Urinary titratable acid and ammonium were not influenced by PTH in group II. In group III, plasma HCO3 was progressively increased from 15 to 40 mM/litre. For all plasma values exceeding 22 mM/litre, HCO3 reabsorption was 1 mM/litre of filtrate lower in the left than in the right kidney. Glomerular filtration and renal plasma flow remained constant during PTH.The results indicate that PTH affects sodium and hydrogen excretion in a very modest fashion. Bicarbonaturia obtains whenever plasma HCO3 exceeds 22 mM/litre during PTH. This phenomenon is associated with a demonstrable reduction in tubular HCO3 reabsorption per unit of filtrate.