Parathyroid hormone interferes with extrarenal disposition of potassium in chronic renal failure.

Available data suggest that the permeability of cellular membranes to potassium is affected by cytosolic calcium. Parathyroid hormone (PTH) has a calcium ionophoric property; it enhances calcium entry into many cells and it increases calcium content in a variety of tissues. Therefore, it is possible that clinical states with excess PTH may affect potassium homeostasis. The present study examined the effect of secondary hyperparathyroidism of chronic renal failure (CFR) on extrarenal potassium disposition of intravenous KCl load in rats with CRF. Experiments were performed after 21-26 days of CRF produced by 7/8 nephrectomy in rats with intact parathyroid glands (CRF control), in normocalcemic parathyroidectomized CRF animals (CFR-PTX) and in adrenalectomized CRF rats (CRF-ADX) maintained with DOCA. The effects of treatment with calcium channel blocker, verapamil, and of PTH administration were also examined. The baseline plasma concentrations of potassium in CRF-PTX rats and in CRF control animals treated with verapamil were significantly (p less than 0.01) lower than those with CRF control and CRF-ADX rats. At the end of 90 min of KCl infusion, the plasma concentrations of potassium as well as the changes from baseline were significantly (p less than 0.01) higher in CRF animals with secondary hyperparathyroidism (CRF control and CRF-ADX) and in those treated with PTH (CRF control with PTH and CRF-PTX with PTH) than in those without secondary hyperparathyroidism CRF-PTX and in those with secondary hyperparathyroidism but treated with verapamil (CRF control with verapamil and CRF-ADX with verapamil).(ABSTRACT TRUNCATED AT 250 WORDS)