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Calcium Channel Blockers; Types, Side Effects, Interactions

Calcium channel blockers or calcium channel antagonists or calcium antagonists are several medications that disrupt the movement of calcium (Ca ²⁺ ) through calcium channels. It is prescription medications that relax blood vessels and increase the supply of blood and oxygen to the heart while also reducing the heart’s workload. Calcium-channel blockers bind to L-type calcium channels located on the vascular smooth muscle, cardiac myocytes, and cardiac nodal tissue (sinoatrial and atrioventricular nodes). These channels are responsible for regulating the influx of calcium into muscle cells.

N-type, L-type, and T-type voltage-dependent calcium channels are present in the zona glomerulosa of the human adrenal, and CCBs can directly influence the biosynthesis of aldosterone in adrenocortical cells, with consequent impact on the clinical treatment of hypertension with these agents.CCBs have been shown to be slightly more effective than beta blockers at lowering cardiovascular mortality, but they are associated with more side effects. Potential major risks, however, were mainly found to be associated with short-acting CCBs.

Types of Calcium Channel Blockers

Dihydropyridine

Dihydropyridine (DHP) calcium channel blockers are derived from the molecule dihydropyridine and often used to reduce systemic vascular resistance and arterial pressure. This CCB class is easily identified by the suffix “-dipine”.

Amlodipine
Aranidipine
Azelnidipine
Barnidipine
Benidipine
Cilnidipine
Clevidipine
Efonidipine
Felodipine
Isradipine
Lacidipine
Lercanidipine
Manidipine
Nicardipine
Nifedipine
Nilvadipine
Nimodipine This substance can pass the blood-brain barrier and is used to prevent cerebral vasospasm.
Nisoldipine
Nitrendipine
Pranidipine

Non-dihydropyridine

Fendiline
Gallopamil
Verapamil

Benzothiazepine

The structural formula of diltiazem

Diltiazem (also used experimentally to prevent a migraine)

Nonselective

While most of the agents listed above are relatively selective, there are additional agents that are considered nonselective. These include mibefradil, bepridil, flunarizine, fluspirilene, and fendiline.

Mechanism of Action of Calcium Channel Blockers

A calcium channel embedded in a cell membrane.

In the body’s tissues, the concentration of calcium ions (Ca²⁺) outside of cells is normally about 10000-fold higher than the concentration inside of cells. Embedded in the membrane of some cells are calcium channels. When these cells receive a certain signal, the channels open, letting calcium rush into the cell. The resulting increase in intracellular calcium has different effects in different types of cells. Calcium channel blockers prevent or reduce the opening of these channels and thereby reduce these effects. Several types of calcium channels occur, with a number of classes of blockers, but almost all of them preferentially or exclusively block the L-type voltage-gated calcium channel. Voltage-dependent calcium channels are responsible for excitation-contraction coupling of skeletal, smooth, and cardiac muscle and for regulating aldosterone and cortisol secretion in endocrine cells of the adrenal cortex. In the heart, they are also involved in the conduction of the pacemaker signals. CCBs used as medications primarily have four effects:

By acting on vascular smooth muscle, they reduce contraction of the arteries and cause an increase in arterial diameter, a phenomenon called vasodilation(CCBs do not work on venous smooth muscle).
By acting on cardiac muscles (myocardium), they reduce the force of contraction of the heart.
By slowing down the conduction of electrical activity within the heart, they slow down the heart beat.
By blocking the calcium signal on adrenal cortex cells, they directly reduce aldosterone production, which correlates to lower blood pressure.

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Since blood pressure is in intimate feedback with cardiac output and peripheral resistance, with relatively low blood pressure, the afterload on the heart decreases; this decreases how hard the heart must work to eject blood into the aorta, so the amount of oxygen required by the heart decreases accordingly. This can help ameliorate symptoms of ischaemic heart disease such as angina pectoris.