alcium channel blockers (CCBs) are a class of drugs and natural substances that disrupt the calcium (Ca2+) through calcium channels.
It has effects on many excitable cells of the body, such as cardiac muscle, i.e. heart, smooth muscles of blood vessels, or neurons. Drugs used to target neurons are used as antiepileptics and are not covered in this article.
The most widespread clinical usage of calcium channel blockers is to decrease blood pressure in patients with hypertension, with particular efficacy in treating elderly patients. Also, calcium channel blockers frequently are used to control heart rate, prevent cerebral vasospasm, and reduce chest pain due to angina pectoris.
Most calcium channel blockers decrease the force of contraction of the myocardium (muscle of the heart). This is known as the negativeinotropic effect of calcium channel blockers. It is because of the negative inotropic effects of most calcium channel blockers that they are avoided (or used with caution) in individuals with cardiomyopathy.
Many calcium channel blockers also slow down the conduction of electrical activity within the heart, by blocking the calcium channel during the plateau phase of the action potential of the heart (see: cardiac action potential). This results in a negative chronotropic effect resulting in a lowering of the heart rate and the potential for heart block. The negative chronotropic effects of calcium channel blockers make them a commonly used class of agents in individuals with atrial fibrillation or flutter in whom control of the heart rate is an issue. Negative chronotropy can be beneficial in that elevated heart rate can result in significantly higher 'cardiac work', which can result in anginal symptoms: lower heart rates represent lower cardiac oxygen requirements.
Pharmacologic Beta blockade is superior to Calcium channel blockade regarding chronotropic properties of the myocardium. Titration of aBeta Blocker to a desired heart rate is decidedly easier than titration of a non-dihydropyridine CCB.
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 the vascular 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 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 ischemic heart disease such as angina pectoris.
Unlike β-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 β-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 β-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, dietary supplements of magnesium oxide and other magnesium preparations may increase or enhance the effects of calcium channel blockade.
All the selective calcium channel blockers are well absorbed after oral administration, although there are marked differences in oral bioavailability that relate to differences in first-pass metabolism. Verapamil and isradipine undergo fairly extensive first-pass metabolism, whereas diltiazem, nifedipine, and nicardipine do not. Protein binding percentages are higher with the dihydropyridines than with either diltiazem or verapamil. With nifedipine and possibly other dihydropyridines, protein binding is concentration dependent, allowing for the possibility of protein-binding interactions, although none of clinical significance has been reported. With verapamil and diltiazem, protein binding is independent of drug concentrations, making displacement interactions unlikely.
Because the older calcium channel blockers have relatively short half-lives, extended-release formulations have been developed to permit once- or twice-daily administration. Isradipine, felodipine, and amlodipine have substantially longer elimination half-lives, although only amlodipine's half-life allows once-daily administration.
What are the side effects of calcium channel blockers?
· The most common side effects of CCBs are constipation, nausea, headache,rash, edema (swelling of the legs with fluid), low blood pressure, drowsiness, and dizziness.
· Liver dysfunction and over growth of gums may also occur. When diltiazem (Cardizem) or verapamil (Calan, Isoptin) are given to individuals with heart failure, symptoms of heart failure may worsen because these drugs reduce the ability of the heart to pump blood.
· Like other blood pressure medications, CCBs are associated with sexual dysfunction.
channel blockers belong to a class of medications that are used to treat a variety of illnesses and conditions. These drugs, also known as calcium antagonists, prevent calcium from infiltrating the cells of the heart and blood vessel walls, according to MayoClinic.com. Their impact on muscle cells in arterial walls allows blood vessels to relax and dilate, easing stress on the circulatory system and relieving conditions in which is a factor.