Endothelial vasodilatory function and blood pressure response to local and systemic hypercalcemia.
BACKGROUND: Endothelial vasodilatory dysfunction occurs in primary hyperparathyroidism. Mechanistically it could be a sign of atherosclerosis, but improvement after parathyroidectomy suggests coupling to hypercalcemia and increased parathyroid hormone levels of patients. METHOD: A total of 12 volunteers underwent forearm venous occlusion plethysmography with systemic (intravenous) and local (brachial artery) infusion of calcium. Endothelium-dependent and endothelium-independent vasodilations were evaluated at stable hypercalcemia through infusion of methacholine and nitroprusside into the brachial artery, and an endothelial function index was calculated as the ratio between them. RESULTS: Normal ionized blood calcium values rose 0.24 +/- 0.09 mmol/L in the cubital venous blood during local calcium infusion and 0.32 +/- 0.16 mmol/L during the systemic infusion. The systemic infusion raised systolic blood pressure (114 +/- 13 to 121 +/- 10 mm Hg; P < .05). It decreased the function index (1.28 +/- 0.40 to 1.00 +/- 0.14; P < .05; n = 11) due to an elevated endothelium-independent vasodilation (EIDV) (P < .05), despite the fact that serum parathyroid hormone values decreased (P< .01). A similar trend in vasodilatory responses was seen during local calcium infusion when the function index correlated inversely to the local blood calcium (r = -0.58, P < .05; n = 12). CONCLUSIONS: Acute hypercalcemia results in dose-related impairment in endothelial vasodilatory function and increased systolic blood pressure. This substantiates the importance of hypercalcemia for cardiovascular complications and prospects for normalization by active treatment in primary hyperparathyroidism.