MedStudentt
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So, I know that calcium channel blockers act on L-type calcium channels preventing calcium entry meaning that calcium cannot bind to the ryanodine/dihydropyridine receptors on the SR.
And I also believe they dilate coronary arteries, but how do they do so?

And how do they decrease preload? Is it related to the lower pressure?
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ahorey
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They block calcium entry into vascular and cardiac cells which reduces calcium intracellularly, causing relaxation and vasodilation of smooth arterial muscle which lowers arterial pressure.
So in the heart it reduces myocardial contractibility ie. reduces conduction speed.
This causes reduced after load (from the vasodilation/reduced HR/Reduced contraction) and therefore lowers myocardial oxygen demand.

there are 2 types, one that is cardio-selective and one vascular selective.

Hope that helps
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MedStudentt
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(Original post by ahorey)
They block calcium entry into vascular and cardiac cells which reduces calcium intracellularly, causing relaxation and vasodilation of smooth arterial muscle which lowers arterial pressure.
So in the heart it reduces myocardial contractibility ie. reduces conduction speed.
This causes reduced after load (from the vasodilation/reduced HR/Reduced contraction) and therefore lowers myocardial oxygen demand.

there are 2 types, one that is cardio-selective and one vascular selective.

Hope that helps
/
Thanks for your response, but I was asking why it would decrease preload?
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ahorey
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The vasodilation of arteries which reduces blood pressure within arteries so reduces/slows venous return to the heart.

however the main action is to reduce after load, so the resistance of blood ejected is reduced.
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macpatgh-Sheldon
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As ahorey says in his/her 2nd post, pre-load is a function of venous return to the heart and atrial compliance.

The vasodilatation of the arterioles (strictly that of venules) brought about by relaxation of the smooth muscle in the tunica media results in peripheral (venous) pooling of blood, thus reducing venous return. The primary effect of various dihydropyridine calcium channel blockers (nifedipine, nicardipine, isradipine, amlodipine, etc.) is on arterioles, but there is a degree of variability in the effect on venules depending on the particular drug. e.g. nifedipine has a greater effect on venules than the very recent clevidipine, so the former would be expected to reduce pre-load to a greater extent than the latter [this might be the result of an extra methyl group [-CH3] on the hydrocarbon chain attached to one of the two aromatic rings that are present in this group of Ca channel blockers].

The other chemical classes of calcium channel blockers, of which verapamil and diltiazem are examples, appear to have little or no effect on venules, so any effect on pre-load is questionable.

M (clinical pharmacologist)
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