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.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Research Project (R01)
Project #
5R01HL037761-02
Application #
3353742
Study Section
(SRC)
Project Start
1986-09-30
Project End
1989-09-29
Budget Start
1987-09-30
Budget End
1988-09-29
Support Year
2
Fiscal Year
1987
Total Cost
Indirect Cost
Name
University of Texas Medical Br Galveston
Department
Type
Schools of Medicine
DUNS #
041367053
City
Galveston
State
TX
Country
United States
Zip Code
77555
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DiPette, D J; Greilich, P E; Nickols, G A et al. (1990) Effect of dietary calcium supplementation on blood pressure and calciotropic hormones in mineralocorticoid-salt hypertension. J Hypertens 8:515-20
DiPette, D J; Greilich, P E; Kerr, N E et al. (1989) Systemic and regional hemodynamic effects of dietary calcium supplementation in mineralocorticoid hypertension. Hypertension 13:77-82
DiPette, D J; Schwarzenberger, K; Kerr, N et al. (1989) Dose-dependent systemic and regional hemodynamic effects of calcitonin gene-related peptide. Am J Med Sci 297:65-70
DiPette, D J; Westlund, K N; Holland, O B (1988) Dietary calcium modulates spinal cord content of calcitonin gene-related peptide in the rat. Neurosci Lett 95:335-40
Breslau, N A (1987) Update on secondary forms of hyperparathyroidism. Am J Med Sci 294:120-31