Abstract
DISTURBANCES of calcium metabolism have been reported in both patients and animals with hypertension. In the experimental model, the abnormalities have included chronic depression of serum ionized calcium concentrations1 , 2 associated with elevated levels of parathyroid hormone,2 altered membrane binding of calcium,3 4 5 6 7 8 9 increased intestinal transport of calcium,10 hypcrcalciuria,2 and the development of nephrolithiasis.11 Similarly, enhanced parathyroid function, lower serum phosphorus concentration, and hypercalciuria12 , 13 have been reported in patients with essential hypertension. In both spontaneously hypertensive rats and patients, extracellular total calcium concentrations are similar to those in their respective normotensive controls.1 , 2 , 13 , 14 The present study was intended to extend our understanding of . . .