The hypothesis that chronic
metabolic acidosis encountered in some patients with
primary hyperparathyroidism is due to inhibition of proximal HCO3 reabsorption has recently been challenged. Indeed, this action of
parathyroid hormone (PTH) has only been observed in acute studies, whereas in animal models of chronic
hyperparathyroidism a metabolic
alkalosis has been induced, probably owing to the release of alkaline
salts from bone tissue, and to the stimulation of tubular
acid secretion by hypercalcaemia. Studies were, therefore, performed to determine the effect of PTH on the renal handling of HCO3 in an animal model in which changes in plasma
calcium and
phosphate, and
nephrocalcinosis, all known to affect tubular acidification, did not occur. Thyroparathyroidectomized (TPTX) rats were infused with synthetic bovine
hormone fragment
bPTH 1-34 via Alzet minipumps at the rate of 0.7 U h-1 to simulate normal endogenous production of PTH (group I) and at the three-fold higher rate of 2.1 U h-1 (group II). In order to prevent changes in serum
calcium and
phosphate, and
nephrocalcinosis, animals of group II were fed a Ca- and P-free diet prior to TPTX (compared with a regular diet for group I) and both groups were treated with
dichloromethylene-diphosphonate (
Cl2MDP, 10 mg kg-1 day-1) and a Ca-free diet during PTH infusion. During the course of PTH infusion both groups of animals had stable and normal levels of plasma
calcium and
phosphate.(ABSTRACT TRUNCATED AT 250 WORDS)