Related Experiment Videos
Calcium supplementation in salt-dependent hypertension
Insights
Calcium supplementation may lower blood pressure in salt-dependent hypertension. This study found that calcium loading reduced salt-induced blood pressure increases and improved sodium excretion in patients and rats.
Area of Science:
- Cardiovascular Physiology
- Mineral Metabolism
- Hypertension Research
Background:
- Salt intake is a major factor in essential hypertension.
- Calcium's role in blood pressure regulation is not fully understood.
- Deoxycorticosterone acetate (DOCA)-salt hypertension in rats mimics human salt-dependent hypertension.
Purpose of the Study:
- To investigate the antihypertensive mechanism of oral calcium loading.
- To assess the effect of calcium supplementation on salt-induced blood pressure elevation.
- To explore calcium's impact on sodium balance and sympathetic activity.
Main Methods:
- Human study: Compared blood pressure response to high salt diet in calcium-supplemented vs. calcium-restricted hypertensive patients.
- Animal study: Evaluated the effect of high calcium intake on DOCA-salt hypertensive rats.
- Measurements included blood pressure, weight gain, urinary sodium excretion, red cell magnesium, and cardiac catecholamines.
Main Results:
- Calcium supplementation significantly attenuated salt-induced blood pressure increases in hypertensive patients.
- High calcium intake reduced blood pressure elevation and sodium retention in DOCA-salt rats.
- Calcium loading increased urinary sodium excretion and red cell magnesium in patients.
- Calcium supplementation decreased cardiac catecholamine levels and improved survival rates in rats.
Conclusions:
- Oral calcium loading may prevent blood pressure rise in salt-dependent hypertension by promoting natriuresis and reducing sodium retention.
- Altered intracellular magnesium levels and normalized sympathetic nervous activity may contribute to calcium's antihypertensive effects.
Abstract:
To clarify the mechanism of the antihypertensive effect of oral Ca loading, we studied the effect of Ca supplementation on salt-induced blood pressure elevations in patients with essential hypertension and DOCA-salt hypertensive rats. When the diet was changed from low to high salt (300 mEq/day), the percent increase in mean blood pressure was smaller (p less than 0.01) in the Ca-supplemented (2,160 mg/day) patients than in the Ca-restricted (250 mg/day) ones. Oral Ca loading resulted in a smaller weight gain, a greater urinary sodium excretion, and an increase in red cell Mg. In the experimental study, high Ca (4% CaCl2) intake attenuated the blood pressure elevation in DOCA-salt-treated rats, accompanied with an increase in urinary sodium excretion, with the resultant attenuation in intra- and extracellular sodium retention. The decrease in catecholamine contents of hearts was improved, and a higher survival rate was observed in Ca-supplemented DOCA-salt rats. The results suggest that Ca supplementation may prevent a rise in BP in salt-dependent hypertension by inducing natriuresis with the resultant attenuation in sodium retention. The altered intracellular Mg level in hypertensive patients and the normalization of enhanced sympathetic nervous activity in DOCA-salt rats may, in part, be involved in its mechanism.