A calcium channel blocker (CCB) is a chemical that disrupts the movement of calcium (Ca ) through calcium channels.

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CCB drugs devised to target neurons are used as antiepileptics . However, the most widespread clinical usage of calcium channel blockers [2] is to decrease blood pressure in patients with hypertension. CCBs are particularly efficacious in treating elderly patients. Calcium channel blockers are also frequently used to alter heart rate, to prevent cerebral vasospasm, and to reduce chest pain caused by angina pectoris. Despite their [3] effectiveness, CCB's often have a high mortality rate over extended periods of use, and have been known to have multiple side effects.

Mechanism of action
Calcium channel blockers work by blocking voltage-gated calcium channels (VGCCs) in cardiac muscle and blood vessels. This decreases intracellular calcium leading to a reduction in muscle contraction. In the heart, a decrease in calcium available for each beat results in a decrease in cardiac contractility. In blood vessels, a decrease in calcium results in less contraction of thevascular smooth muscle and therefore an increase in arterial diameter (CCBs do not work on venous smooth muscle), a phenomenon called vasodilation. Vasodilation decreases total peripheral resistance, while a decrease in cardiac contractility decreases cardiac output. Since blood pressure is determined by cardiac output and peripheral resistance, blood pressure drops. Calcium channel blockers are especially effective against large vessel stiffness, one of the common causes of elevated systolic blood [2] pressure in elderly patients. With a relatively low blood pressure, the afterload on the heart decreases; this decreases how hard the heart must work to eject blood into the aorta, and so the amount of oxygen required by the heart decreases accordingly. This can help ameliorate symptoms of ischaemic heart disease such as angina pectoris. Unlike beta blockers, calcium channel blockers do not decrease the responsiveness of the heart to input from the sympathetic nervous system. Since moment-to-moment blood pressure regulation is carried out by the sympathetic nervous system (via the baroreceptor reflex), calcium channel blockers allow blood pressure to be maintained more effectively than do beta blockers. However, because calcium channel blockers result in a decrease in blood pressure, the baroreceptor reflex often initiates a reflexive increase in sympathetic activity leading to increased heart rate and contractility. A beta blocker may be combined with a dihydropyridine calcium channel blocker to minimize these effects. Ionic calcium is antagonized by magnesium ions in the nervous system. Because of this, bioavailable supplements of magnesium, possibly including magnesium chloride, magnesium lactate and magnesium aspartate, may increase or enhance the effects of calcium channel blockade.[4] Mechanism of action These substances are AT1-receptor antagonists – that is, they block the activation of angiotensin II AT1 receptors. Blockage of AT1 receptors directly causes vasodilation, reduces secretion ofvasopressin, and reduces production and secretion of aldosterone, amongst other actions. The combined effect reduces blood pressure. The specific efficacy of each ARB within this class depends upon a combination of three pharmacodynamic and pharmacokinetic parameters. Efficacy requires three key PD/ PK areas at an effective level; the parameters of the three characteristics will need to be compiled into a table similar to one below, eliminating duplications and arriving at consensus values; the latter are at variance now.

Mechanism of action
Angiotensin-converting enzyme inhibitors reduce the activity of the renin-angiotensin-aldosterone system. ACE inhibitors block the conversion of angiotensin I to angiotensin II.

Mechanism action of beta blockers They have proven to reduce the onset of heart attacks

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