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Calcium in the pathogenesis and therapy of human hypertension
Insights
Calcium plays a key role in regulating blood pressure. Abnormal calcium handling is linked to hypertension, and calcium channel blockers offer a targeted therapy with no significant metabolic side effects.
Area of Science:
- Cardiovascular Physiology
- Nephrology
- Pharmacology
Background:
- Epidemiologic data link abnormal calcium homeostasis to hypertension and cardiovascular disease risk.
- Cellular calcium handling defects are implicated in the development and progression of hypertension.
- Dietary and environmental factors may influence calcium's role in blood pressure regulation.
Purpose of the Study:
- To review the contribution of calcium to normal blood pressure regulation.
- To explore the role of cellular calcium handling defects in hypertension.
- To evaluate calcium channel blockers as a specific therapy for hypertension.
Main Methods:
- Review of epidemiologic data on calcium and hypertension.
- Analysis of recent studies on cellular calcium handling in experimental and human hypertension.
- Examination of clinical trial data for oral calcium channel blockers like nifedipine.
Main Results:
- Calcium channel blockers, such as nifedipine, rapidly reduce peripheral vascular resistance and mean arterial pressure upon oral administration.
- Cardiac output and renal perfusion are maintained during treatment with these agents.
- Long-term use of calcium channel blockers does not lead to significant adverse metabolic effects or biochemical changes, unlike other antihypertensives.
Conclusions:
- Defects in cellular calcium handling contribute to elevated arterial blood pressure in hypertension.
- Calcium channel blockers represent a specific therapeutic approach for hypertension by addressing these cellular defects.
- Calcium channel blockers offer a favorable metabolic profile compared to other antihypertensive medications.
Abstract:
The contribution of calcium to normal regulation of blood pressure is reviewed. Epidemiologic data suggest that abnormal calcium homeostasis may play a role in dietary and environmental contributions to the risk of hypertension and cardiovascular disease. Recent studies in human and experimental hypertension point to one or more defects in cellular handling of calcium as contributing to the initiation and maintenance of increased vascular tone and, thereby, to abnormally elevated arterial blood pressure. By "correcting" some of these defects, calcium channel blockers may represent relatively specific therapy for hypertension. Data from human trials are still limited, but it is evident that, following oral administration of nifedipine and related compounds, an immediate decrease in peripheral vascular resistance and mean arterial pressure is produced. Cardiac output is not altered, and renal perfusion is maintained. In contrast to many currently used antihypertensive agents--including thiazide diuretics and beta blockers--which frequently induce alterations in the patient's serum chemical values, long-term administration of calcium channel blockers does not produce significant adverse metabolic effects or substantive changes in biochemical parameters.
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