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Updated: Oct 13, 2026
Fluorescence-based Measurement of Store-operated Calcium Entry in Live Cells: from Cultured Cancer Cell to Skeletal Muscle Fiber
Published on: February 13, 2012
Insights
Coronary vasospasm causes ischemic pain in some atherosclerosis patients. Calcium entry blockers like verapamil and diltiazem prevent this spasm via distinct mechanisms, offering varied therapeutic benefits.
Area of Science:
- Cardiology
- Pharmacology
Background:
- Coronary vasospasm is increasingly recognized as a cause of myocardial ischemic pain in patients with coronary atherosclerosis.
- This vasospasm, affecting 27-35% of patients with angina at rest, is triggered by normal stimuli leading to coronary artery spasm.
- Evidence suggests increased intracellular calcium release from sarcolemmal sites may cause this spasm.
Purpose of the Study:
- To investigate the mechanisms by which calcium entry blockers prevent coronary vasospasm.
- To compare the distinct mechanisms of action of verapamil and diltiazem in reducing intracellular calcium.
- To highlight the differential effects of these agents on cardiac function and their suitability for various clinical conditions.
Main Methods:
- The study reviews existing evidence on the role of calcium in coronary vasospasm.
- It analyzes the pharmacological actions of calcium entry blockers, specifically verapamil and diltiazem.
- Comparative analysis of their effects on intracellular calcium levels, sarcolemmal stores, and ion transport mechanisms.
Main Results:
- Calcium entry blockers are effective in preventing coronary spasm by reducing intracellular calcium.
- Verapamil directly reduces intracellular and sarcolemmal calcium stores.
- Diltiazem reduces intracellular calcium by stimulating the sodium-potassium pump, enhancing sodium-calcium exchange.
Conclusions:
- Verapamil and diltiazem employ different mechanisms to combat coronary vasospasm.
- Their distinct effects on myocardial contractility, cardiac conduction, and vascular smooth muscle influence their clinical applications.
- These differences make specific calcium entry blockers more suitable for treating conditions like angina, tachycardia, hypertension, and hypertrophic cardiomyopathy.
Abstract:
Recently it has been recognized that coronary vasospasm plays a significant role in precipitating myocardial ischemic pain in a significant minority of individuals with coronary atherosclerosis (approximately 27-35% of patients with angina pectoris at rest). In these individuals normal physiological vasoconstrictor stimuli appear to trigger a spasm of the large epicardial coronary vessels; evidence suggests that it may be caused by the release of increased amounts of calcium from augmented sarcolemmal storage sites. The calcium entry blockers are remarkably effective in preventing coronary spasm by reducing intracellular calcium, but by different mechanisms. Verapamil appears to reduce intracellular and, more specifically, sarcolemmal calcium stores directly. Diltiazem appears to reduce intracellular calcium by stimulating the sarcolemmal sodium-potassium pump and reducing intracellular sodium, and by this mechanism. potentiating passive sodium-calcium exchange. The effects of the calcium entry blockers on myocardial contractility, cardiac pacemaker and conduction tissue, and regional vascular smooth muscle are also different. This makes some of these agents more suitable than others for therapy of other clinical problems such as chronic stable angina pectoris, supraventricular tachycardia, hypertension, hypertropic cardiomyopathy, and protection of the ischemic myocardium during cardiac surgery.
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