High Blood Pressure Treatment (cont.)

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Calcium channel blockers (CCBs)

Calcium channel blockers inhibit the movement of calcium into the muscle cells of the heart and arteries. Calcium is needed for these muscles to contract. Calcium channel blockers lower blood pressure by decreasing the force of the heart's pumping action and relaxing the muscle cells in the walls of the arteries.

Three major types of calcium channel blockers are used. One type is the dihydropyridines, which do not slow the heart rate or cause other abnormal heart rates or rhythms (cardiac arrhythmias). These drugs include amlodipine (Norvasc), sustained release nifedipine (Procardia XL, Adalat CC), felodipine (Plendil), and nisoldipine (Sular).

The other two types of calcium channel blockers are referred to as the non-dihydropyridine agents. One type is verapamil (Calan, Covera, Isoptin, and Verelan) and the other is diltiazem (Cardizem, Tiazac, Dilacor, and Diltia). The non-dihydropyridines can cause slowing of the heart rate (bradycardia). The non-dihydropyridines are not recommended in congestive heart failure. Both the dihydropyridines and the non-dihydropyridines are very useful when used alone or in combination with other antihypertensive agents.

Many of the calcium channel blockers come in a short-acting form and a long-acting (sustained release) form. The short-acting forms of the calcium channel blockers may have adverse long-term consequences, such as strokes or heart attacks. These effects are due to the wide fluctuations in the blood pressure and heart rate that occur during treatment resulting from the rapid onset and short duration of the short-acting compounds. When the calcium channel blockers are used in sustained release preparations less fluctuation occurs. The sustained release forms of calcium channel blockers are probably safer for long-term use. The main side effects of these drugs include constipation, swelling (edema), and a slow heart rate (only with the non-dihydropyridine types).

Medically Reviewed by a Doctor on 10/11/2012

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