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Calcium and blood pressure regulation in normal and hypertensive subjects
Insights
Acute hypercalcemia increases blood pressure (BP) by boosting adrenergic activity. Calcium inhibition with nifedipine reduces norepinephrine pressor reactivity, impacting BP control mechanisms differently than angiotensin.
Area of Science:
- Cardiovascular Physiology
- Endocrinology
- Pharmacology
Background:
- Calcium plays a role in blood pressure regulation.
- The precise mechanisms of calcium's influence on BP control, particularly involving the adrenergic and angiotensin systems, require further elucidation.
Purpose of the Study:
- To investigate the impact of acute hypercalcemia and calcium inhibition on blood pressure and related hormonal systems.
- To determine whether the adrenergic or angiotensin system is more sensitive to changes in calcium levels.
Main Methods:
- Assessed plasma norepinephrine (NE), epinephrine, renin activity, and angiotensin II (AII) levels.
- Measured cardiovascular pressor responsiveness to NE and AII during induced hypercalcemia and nifedipine treatment.
- Studied normal and borderline hypertensive subjects.
Main Results:
- Acute hypercalcemia significantly increased systolic BP and plasma catecholamines in normal and borderline hypertensive subjects.
- Neither hypercalcemia nor nifedipine significantly altered plasma renin or AII levels.
- Nifedipine reduced BP in borderline hypertensives and decreased NE pressor responses in both groups.
Conclusions:
- Adrenergic BP control appears more sensitive to calcium metabolism variations than the angiotensin system.
- Acute hypercalcemia may elevate BP via increased adrenergic activity.
- Calcium inhibition with nifedipine modulates noradrenergic BP control by reducing NE pressor reactivity.
Abstract:
To elucidate the mechanisms involved in calcium-mediated blood pressure (BP) control, plasma norepinephrine (NE), epinephrine, renin activity, and angiotensin II (AII) levels and the cardiovascular pressor responsiveness to NE and AII were assessed before and during acute mild hypercalcemia or short-term calcium (Ca) inhibition with nifedipine in 20 normal and five borderline hypertensive subjects. In normal subjects, systolic BP and plasma NE and epinephrine concentrations were increased significantly (p less than 0.05) during an acute rise in serum Ca of 3.1 mg/dl (intermediate rate Ca infusion, 0.05 mg/kg/min for 3 hours), but not following an increase of 1 mg/dl (low rate Ca infusion, 0.034 mg/kg/min for 2 hours). In the borderline hypertensive group, low-rate Ca infusion elevating serum Ca by 1 mg/dl was associated with a slight increase in systolic BP (p less than 0.05) and plasma catecholamines. In both groups, the pressor responses to infused NE and AII, and plasma renin and AII levels, were unchanged during mild to moderate hypercalcemia. Nifedipine given for 2 weeks (average dose, 48 mg/d) reduced BP significantly (p less than 0.05) in the borderline hypertensive subjects only and NE pressor responses in both groups (p less than 0.025), but had no significant effect on plasma catecholamines, renin, or AII levels. These findings suggest that the adrenergic BP control mechanism may be more dependent on clinical variations in calcium metabolism than the angiotensin BP regulatory mechanism. Acute hypercalcemia may increase BP at least in part by causing an increase in adrenergic activity without an equivalent decrease in cardiovascular reactivity. Calcium inhibition with nifedipine may modify noradrenergic BP control by lowering the NE pressor reactivity without causing an equivalent increase in adrenergic activity.