The present investigation examined the possible influence of urinary c
alcium excretion on the concentration of renal calbindin-D28k. Thiazid
e diuretics stimulate calcium transport across the epithelial cells of
the distal tubule, which express calbindin-D28k in high concentration
s. Calbindin-D28k is assumed to facilitate transcellular Ca diffusion.
Reduced urine calcium excretion and increased urine output were induc
ed in Wistar rats by infusion of bendroflume-thiazide 1 mg/kg/day. The
two control groups had infusions of either furosemide 20 mg/kg/day or
vehicle. n = 8 in each group. Urinary Ca excretion was reduced to 10%
in the thiazide group and increased by 50% in the furosemide group. l
ienal concentrations of calbindin-D28 showed no difference between veh
icle, thiazide- and furosemide-treated rats. No differences in plasma
concentrations of calcium, magnesium, phosphorus, urea, PTH, calcitoni
n and 1,25-(OH)(2)D were found between the groups. The present study d
escribes that urine calcium excretion selectively can be manipulated w
ithout accompanying changes in renal calbindin-D28k concentrations. Th
e data, therefore, suggest that urinary calcium excretion is not a sig
nificant determinator of cytosolic concentrations of renal calbindin-D
28k.