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 KC1 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 DOC A. 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 < 0.01) lower than those with CRF control and CRF-ADX rats. At the end of 90 min of KC1 infusion, the plasma concentrations of potassium as well as the changes from baseline were significantly (p < 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). The percents of potassium load translocated from extracellular space to cells in CRF-PTX rats (80 ± 4.4%), in CRF control rats with verapamil (79 ± 2.3%) and in CRF-ADX rats with verapamil (76 ± 1.4%) were significantly (p < O.Ol) higher than those in CRF control animals (67 ± 2.8%), in CRF control rats treated with PTH (59 ± 0.9%), in CRF-PTX animals treated with PTH (60 ± 2.0%) and in CRF-ADX rats (65 ± 1.4%). The data show that the state of secondary hyperparathyroidism of CRF interferes with extrarenal disposal of potassium. This derangement could be prevented by parathyroidectomy or by treatment with verapamil. Our results are consistent with the notion that this effect of excess PTH is mediated by the calcium ionophoric property of the hormone.