Elevated blood levels of cytosolic calcium--[Ca2+]i--appear to mediate the downregulation of the mRNA of the PTH-PTHrP receptor in states with chronic elevation of blood levels of parathyroid hormone (PTH). Data on the effect of hypoparathyroidism on basal levels of [Ca2+]i are not available, while those on the mRNA of the PTH-PTHrP receptor are variable. The present study was performed to measure [Ca2+]i in renal cells, to estimate the concentrations of mRNA of the PTH-PTHrP receptor in kidney, liver, and heart, and to examine the phosphaturic response to PTH and adenine 3',5'-cyclic monophosphate (cAMP) in normal rats as well as in animals after 3 weeks of parathyroidectomy (PTX). The basal levels of [Ca2+]i of the renal proximal tubular cells in PTX animals (163 +/- 5.1 nM) were not different from those in normal rats (160 +/- 4.9 nM). The concentrations of the mRNAs of the PTH-PTHrP receptor in kidney, liver, and heart were not upregulated after PTX. The phosphaturic responses to PTH or cAMP in normal and PTX rats were not different. The results show that PTX of rats with the consequent decrease in their blood levels of PTH is not associated with changes in the basal levels of [Ca2+]i, the concentrations of the mRNA of the PTH-PTHrP receptor, and in the phosphaturic response to PTH. These data lend support to the notion that the regulation of the mRNA of the PTH-PTHrP receptor in the presence of excess PTH or its lack is mediated through changes in basal levels of [Ca2+]i.