Felodipine
decreases arterial smooth muscle contractility and subsequent vasoconstriction
by inhibiting the influx of calcium ions through voltage-gated L-type calcium
channels. It reversibly competes against nitrendipine and other DHP CCBs for
DHP binding sites in vascular smooth muscle and cultured rabbit atrial cells.
Calcium ions entering the cell through these channels bind to calmodulin.
Calcium-bound calmodulin then binds to and activates myocin light chain kinase
(MLCK). Activated MLCK catalyzes the phosphorylation of the regulatory light
chain subunit of myocin, a key step in muscle contraction. Signal amplification
isachieved by calcium-induced calcium release from the sarcoplasmic reticulum
through ryanodine receptors. Inhibition of the initial influx calcium decreases
the contractile activity of arterial smooth muscle cells and results in
vasodilation. The vasofilatory effects of felodipine result in an overall
decrease in blood pressure. Felodipine may be used to treat mild to moderate
essential hypertension.
Reference: Tripathi KD;
Essentials of Clinical Pharmacology; Jaypee Brothers Medical Publishers;
seventh edition; Page no:
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