What is the mechanism of action of a calcium channel blocker on the heart?

Question

Have cardiac test -- can someone simplify what a calcium channel blocker does. The book is confusing!!!

Answer 1

It decreases the amount of calcium in the blood in the arteries and the muscle cells of the heart. Keeps them wider (and "less sticky" and prone to clots and blockages too). Calcium causes a narrowing of the arteries and makes the heart contract harder.
Blockers decrease the amount of calcium, thereby not requiring the heart to work as hard or require as much oxygen. Good for treatment of angina and hypertension.

Answer 2

You're on the right track, but you haven't got it right yet. Calcium is neccessary in muscle fibers (cells) to contract. I believe calcium channel blockers block the entry into smooth muscle cells, in the walls of arterioles, from the plasma. This decreases contraction by these fibers, and thus decreases vasoconstriction. The result is vasodilatation. This expansion of the lumens (the hole inside the small artery on cross section) of arterioles all over the body, decreases peripheral vascular resistance, and this lowers the blood pressure. Whew! These drugs may also decrease the contractility or strength of contraction of the heart, which would tend to lower blood pressure as well. Now as far as the precise subcellular mechanism, I'm a little rusty. I'm sure it's available if you google it in. I'm just giving you what I know as a practicing ER doc. My favorite class of drugs for lowering blood pressure are the ARBs (angiotensin receptor blockers). I don't believe that the calcium channel blockers ever lower the serum calcium. I've never noticed that. I know that if a patient is overdosed on calcium channel blockers, you can reverse it somewhat by giving IV calcium. In addition to their use for lowering blood pressure, some calcium channel blockers are used to slow the ventricular rate in supraventricular tachycardias, such as paroxysmal supraventricular tachycardia, atrial flutter, and atrial fibrillation. We always have some concern with these drugs, if the patient has some heart failure, ie. a weak heart muscle, in that they may decrease the contractility of the heart and throw them into overt heart failure. We don't have that concern with the ACE inhibitors and the ARB's. The ACE inhibitors have a frequent side effect of causing a nagging cough, because they cause a buildup of histamine, but the ARB's don't have that problem.

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Answer 3

Although it is good enough to call them CCB's for the lay public if you are aswering a physiology test it is good to think of their subclasses....i.e the DHP and the Non DHP CCB's (DHP- Dihidropyridine)
Essentially they inhibit passage of calcium through the voltage gated L-type (for Large/Long-lasting current) calcium channel on vascular smooth muscle cells and cardiac myocytes, reducing calcium availability for muscle contraction.
The major clinical use of DHP CCB like amlodipine and Nifedipine is for Hypertension by relaxation of smooth muscle in arteries and arterioles.
The major clinical use of Non DHP's like diltiazem and Verapamil is to slow conduction of the cardiac impulse across the A-V node to decrease the ventricular rate as in Atrial Fibrillation wiht high ventricular rate.
Mention in your test that the CCB's are in general 'Negatively Chronotrophic and Bathmotropic' which is the fancy way of saying " slows the heart and decreases Contractility/myocardial excitability" Medical teachers like big words ;).
Good luck with the test.

Answer 4

they decrease the force of contraction on the myocardium. which in turn lowers blood pressure. also slow the electrical conduction within the heart by blocking calcium channel during the plateau phase of the action potential of the heart. this also causes a lower of the heart rate.

Answer 5

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Answer 6

Ca Channel Blockers have Therapeutic effect for ANGINA and also for HYPERTENSION.

The Mechanisms for both vary slightly.

FOR ANGINA :
The precise mechanisms by which inhibition of calcium influx relieves angina has not been fully determined, but includes at least the following two mechanisms:
1. Relaxation and Prevention of Coronary Artery Spasm
Ca-channel blocker dilates the main coronary arteries and coronary arterioles, both in normal and ischemic regions, and is a potent inhibitor of coronary artery spasm, whether spontaneous or ergonovine-induced. This property increases myocardial oxygen delivery in patients with coronary artery spasm, and is responsible for the effectiveness of nifedipine in vasospastic (Prinzmetal's or variant) angina. Whether this effect plays any role in classical angina is not clear, but studies of exercise tolerance have not shown an increase in the maximum exercise rate-pressure product, a widely accepted measure of oxygen utilization. This suggests that, in general, relief of spasm or dilation of coronary arteries is not an important factor in classical angina.
2. Reduction of Oxygen Utilization
Ca-channel blocker regularly reduces arterial pressure at rest and at a given level of exercise by dilating peripheral arterioles and reducing the total peripheral vascular resistance (afterload) against which the heart works. This unloading of the heart reduces myocardial energy consumption and oxygen requirements, and probably accounts for the effectiveness of nifedipine in chronic stable angina.


FOR HYPERTENSION:
The mechanism by which Ca-channel blocker reduces arterial blood pressure involves peripheral arterial vasodilatation and the resulting reduction in peripheral vascular resistance. The increased peripheral vascular resistance that is an underlying cause of hypertension results from an increase in active tension in the vascular smooth muscle. Studies have demonstrated that the increase in active tension reflects an increase in cytosolic free calcium.
Ca-channel blockers are a peripheral arterial vasodilator which acts directly on vascular smooth muscle. The binding of these drugs to voltage-dependent and possibly receptor-operated channels in vascular smooth muscle results in an inhibition of calcium influx through these channels. Stores of intracellular calcium in vascular smooth muscle are limited and thus dependent upon the influx of extracellular calcium for contraction to occur. The reduction in calcium influx by Ca-channel blockers causes arterial vasodilation and decreased peripheral vascular resistance which results in reduced arterial blood pressure.

(from www.drugs.com)

I HOPE NO MORE CONFUSION NOW ! RIGHT ?