Evidence for a direct effect of parathyroid hormone on urinary acidification

Abstract

The effects of intravenously administered parathyroid extract and of a purified parathyroid hormone on urinary acidification and on solute excretion were measured in six thyroparathyroidectomized dogs, in three normal women, and in a patient with diabetes insipidus. Parathyroid extract and the purified parathyroid hormone produced an immediate rise in urinary pH and bicarbonate with a fall in titratable-acid-minus-bicarbonate and in ammonia in all subjects. This was usually associated with a rise in urinary sodium and potassium. The changes in urinary acidification usually preceded any rise in glomerular filtration rate, and were associated with no increase in serum bicarbonate concentration. They also preceded a rise in the excretion of phosphate in most experiments, and thus did not depend on a rise in urinary buffer content. It is postulated that parathyroid hormone inhibits sodium-for-hydrogen ion exchange in the renal tubules, perhaps by interfering directly with the ability of the kidney to maintain a hydrogen ion gradient between the body fluids and the tubular urine.