Calcium ions are intimately involved in many aspects of cardiovascular function. Modification of calcium homeostasis therefore represents a key target for pharmacological intervention to achieve therapeutic control of hypertension. The calcium channel blockers (CCBs) act by blocking calcium influx through voltage-dependent L (long-acting) channels without affecting calcium release from the sarcoplasmic reticulum. The effect of blocking these channels is a decrease in the intracellular calcium concentration, which reduces vascular smooth muscle tone. The subsequent decrease in peripheral resistance causes a decrease in systemic blood pressure. The CCBs also decrease myocardial contractility, which decreases myocardial oxygen consumption. Overall, the CCBs at therapeutic doses improve the efficiency of ventricular function. They also have a number of other beneficial effects, including an antiprolifera-tive effect. The CCBs in clinical use vary according to their relative selectivi-ties for vascular and cardiac tissue and their applicability to the treatment of hypertension or ischaemic heart disease. The first-generation CCBs (verapam-il, nifedipine and diltiazem) are associated wit
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