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Acute hypercalcemic hypertension in man: role of hemodynamics, catecholamines, and renin
Insights
Acute hypercalcemia significantly elevates blood pressure by increasing peripheral vascular resistance. This hypertension is primarily driven by direct calcium effects on blood vessels, with mild contributions from epinephrine release and plasma volume contraction.
Area of Science:
- Cardiovascular Physiology
- Endocrinology
- Nephrology
Background:
- Hypercalcemia, elevated serum calcium levels, can manifest with various cardiovascular effects.
- Understanding the precise hemodynamic and hormonal changes during acute hypercalcemia is crucial for clinical management.
Purpose of the Study:
- To investigate the impact of acute hypercalcemia on blood pressure, blood volume, and hemodynamic parameters.
- To examine the changes in plasma concentrations of key hormones including norepinephrine, epinephrine, dopamine, renin, and aldosterone during acute hypercalcemia.
Main Methods:
- Ten patients received an intravenous infusion of calcium gluconate over 3 hours.
- Measurements included serum calcium, blood pressure, blood volume, hematocrit, heart rate, cardiac output, total peripheral resistance, and plasma catecholamine and hormone levels.
Main Results:
- Acute hypercalcemia significantly increased systolic and diastolic blood pressure.
- Plasma volume decreased, while hematocrit and total peripheral resistance increased.
- Plasma epinephrine levels rose, but norepinephrine, dopamine, renin, and aldosterone concentrations remained largely unchanged.
Conclusions:
- Acute hypercalcemic hypertension is primarily mediated by an increase in total peripheral resistance.
- Direct effects of calcium on blood vessels likely play a key role.
- Epinephrine release and plasma volume contraction may have minor contributory or inhibitory roles, respectively.
Abstract:
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.