Polyethylene glycol (PEG) has been used to investigate the physiological basis of sodium intake because it sequesters sodium from the extracellular fluid (ECF) and causes rats to drink concentrated NaCl solutions. To test the hypothesis that PEG also depletes ECF calcium and thus activates calcium intake, male Sprague-Dawley rats received two-bottle tests with a choice between a taste solution and water. Relative to intakes after control injections, rats injected with PEG (5 ml of 30% wt/wt sc) drank significantly greater volumes of several calcium solutions (0.1, 1, 10, or 32 mM CaCl2 or 10 or 100 mM calcium lactate). They also drank more 10 mM SrCl2, 300 mM NaCl, and 100 mM KHCO3, drank less 10 mM sodium saccharin, and did not alter intakes of 10 or 100 mM KCl, 32 mM NH4Cl, 10 mM AlCl3, 10 mM FeCl2, 100 mM CaCl2, or 1,000 mM NaCl. Thus PEG treatment produced an appetite that was specific to low and moderate concentrations of calcium, sodium, and perhaps bicarbonate. The physiological basis for this appetite was explored. At 24 h after PEG injection, plasma total calcium concentrations were either unaltered or increased, but plasma ionized calcium concentrations were reduced. Concentrations of parathyroid hormone and calcitonin but not 1 alpha, 25-dihydroxyvitamin D3 were elevated. Perhaps one or more of these changes in calcium homeostasis is responsible for the increased calcium intake. Whatever the mechanism, it is clear that PEG treatment induces an appetite for calcium in addition to the well-known appetite for sodium.