The reason why some hypertensive patients have a blood pressure fall and others have a blood pressure rise with calcium supplementation is unknown. We postulate that hypertensive patients with chronic sodium overload have enhanced urinary calcium excretion, which causes a secondary hyperparathyroidism that amplifies the basic hypertensive process. Other patients may develop secondary hyperparathyroidism from a defect in intestinal calcium absorption. Dietary calcium supplementation may benefit these patients by reducing the secondary hyperparathyroidism. This postulate will be explored by comparing the regulation of calcium homeostasis in hypertensive patients and normal subjects during sodium depletion and sodium loading. The types of hypertensive patients which will be evaluated for evidence of secondary hyperparathyroidism include those with primary aldosteronism, low-renin essential hypertension, and non-modulating, normal-resin essential hypertension. Black vs white racial comparisons will be done to explore the possibility that hypertension in blacks is partially dependent on secondary hyperparathyroidism. Calcium homeostasis will be assessed with determinations of fractional intestinal calcium absorption, serum total and ionized calcium, parathyroid hormone, 1,25-dihydroxyvitamin D3, 25-hydroxyvitamin D3, calcitonin, and gamma carboxyglutamic acid containing protein of bone (GLA) and urinary calcium, cyclic AMP, and hydroxyproline. More accurate assessment of blood pressure changes will be provided by 24 hr ambulatory blood pressure recording. The effects of dietary calcium supplementation on calcium homeostasis and on the blood pressure control will be assessed in these patients. The need for sodium depletion to fully normalize calcium homeostasis will be explored. The effect of enalapril, a converting-enzyme inhibitor, on calcium homeostasis and blood pressure control in non-modulating, normal-renin hypertensives will be determined. In addition, the possibility that calcium supplementation in the presence of sodium depletion may lead to a blood pressure rise in patients with modulating, normal-renin essential hypertension will be evaluated. These studies should increase our understanding of calcium homeostasis in several types of hypertensive patients and thereby lead to diagnostic and therapeutic recommendations for hypertensive patients who may benefit from calcium supplementation.
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