Acute hypercalcemic hypertension in man: role of hemodynamics, catecholamines, and renin.

The effect of acute hypercalcemia on blood pressure, blood volume, hemodynamic parameters, plasma norepinephrine, epinephrine, dopamine, renin, and aldosterone concentrations was investigated. After 1 hour of equilibration, 10 patients received an infusion of calcium gluconate in 5% dextrose (calcium 15 mg/kg of body wt in 3 hours). The calcium infusion increased the mean serum calcium from 8.7 to 13.0 mg/dl, the systolic blood pressure from 144 +/- 10 to 184 +/- (SEM) 12 mm Hg (P less than 0.001), the diastolic pressure from 78 +/- 4 to 93 +/- 5 mm Hg (P less than 0.01). The plasma volume was decreased by 9% (P less than 0.001), whereas the hematocrit was increased (P less than 0.05). Heart rate and cardiac output remained unchanged. Total peripheral resistance was increased from 1643 +/- 223 to 2256 +/- 387 dyne.sec/cm5 (P less than 0.05). The plasma epinephrine concentration rose from 4.5 +/- 0.7 to 6.9 +/- 1.2 ng/dl (P less than 0.01). The plasma norepinephrine concentration was unchanged after 2 hours and increased only slightly after 3 hours of calcium infusion. Plasma renin, aldosterone, and dopamine concentrations were not significantly changed. These findings demonstrate that acute hypercalcemic hypertension is mediated by an increase in peripheral vascular resistance. Hypercalcemic hypertension may be induced by a direct effect of calcium on blood vessels; calcium-mediated increase in adrenal epinephrine release may play a mild contributory role, and plasma volume contraction, an inhibitory role.