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Effect of calcium and calcium blockers in hypertension
Insights
Calcium supplementation may help lower blood pressure in some patients with essential hypertension. Combining calcium with nifedipine further reduced blood pressure in responders, suggesting a potential therapeutic strategy for specific hypertensive individuals.
Area of Science:
- Cardiovascular Medicine
- Nephrology
- Pharmacology
Background:
- Calcium plays a crucial role in arterial smooth muscle function.
- Dysregulation of calcium metabolism is implicated in atherogenesis and hypertension.
- Existing therapies include slow channel inhibitors (e.g., nifedipine) and calcium salts for managing arterial calcium levels in hypertensive patients.
Purpose of the Study:
- To investigate the efficacy of calcium gluconate and its combination with nifedipine in patients with essential hypertension.
- To identify predictors of response to calcium therapy in hypertension.
Main Methods:
- A study involving 41 patients with essential hypertension.
- Patients were divided into responders (n=29) and non-responders (n=12) to calcium gluconate therapy.
- Responders received a single-blind, placebo-controlled trial of combined calcium and nifedipine administration.
Main Results:
- Calcium gluconate therapy reduced blood pressure by 9.8/6.3 mmHg in 29 hypertensive patients.
- Combined calcium and nifedipine administration in responders led to a further significant decrease in blood pressure (9.6/3.2 mmHg).
- Non-obese females with high salt intake showed a better response to calcium therapy.
Conclusions:
- Calcium salts combined with calcium blockers may offer additional blood pressure reduction in a subset of hypertensive patients.
- The positive role of calcium in hypertension management requires further investigation.
- Larger studies are needed to confirm these findings and predict calcium therapy response.
Abstract:
Calcium is important in the maintenance of arterial smooth muscle function and its alteration from normal may predispose to atherogenesis and hypertension. Slow channel inhibitors such as nifedipine and calcium salts have been used separately to modulate arterial calcium in patients with hypertension. This study included 41 patients with essential hypertension, of whom 29 responded to calcium gluconate therapy (9.8/6.3 mmHg) and the remaining 12 (group B) showed either no response or a rise in blood pressure. Combined administration of calcium and nifedipine in responders (29 cases, group A) in a single-blind, placebo-controlled manner showed a further substantial decrease (9.6/3.2 mmHg) in pressure compared with pressures during placebo administration in both short- as well as long-term administration in group B patients. Although it is difficult to predict the positive role of calcium in hypertension, non-obese females with increased salt intake show a greater response to calcium therapy. It is possible that calcium salts plus calcium blocker therapy can further reduce the blood pressure in a particular subset of hypertensives. However, this needs further confirmation in a larger study.