Calcium entry blockers and vascular smooth muscle heterogeneity.
Inasmuch as the cytoplasmic level of activator Ca2+ governs the contractile activity of vascular smooth muscle cells, the efficacy of calcium entry blockers in curtailing vasoconstriction is determined by the dependency of this level on the influx of extracellular Ca2+ into the cells; this dependency varies with the trigger to contraction as well as with the anatomical origin of the vascular preparation tested. Certain calcium entry blockers (e.g., flunarizine and lidoflazine) tested in experimental conditions triggering the influx of the activator ion exhibit a pronounced tissue selectivity, presumably because the characteristics and accessibility of the Ca2+ channels vary among different vascular smooth muscle cells. The time of onset and duration of calcium entry blockade are not identical for all calcium entry blockers, which must reflect their permeation in the tissue as well as their individual pharmacological properties at the molecular level.
D000818:Animals; D002118:Calcium / Q000502:physiology*; D002121:Calcium Channel Blockers / Q000494:pharmacology*; D002936:Cinnarizine / Q000031:analogs & derivatives / Q000494:pharmacology; D005444:Flunarizine; D005711:Gallopamil / Q000494:pharmacology; D008013:Lidoflazine / Q000494:pharmacology; D009119:Muscle Contraction / Q000187:drug effects*; D009131:Muscle, Smooth, Vascular / Q000502:physiology*; D009543:Nifedipine / Q000494:pharmacology; D011817:Rabbits; D014700:Verapamil / Q000494:pharmacology
D002121:Calcium Channel Blockers; D005711:Gallopamil; D002936:Cinnarizine; D014700:Verapamil; D009543:Nifedipine; D008013:Lidoflazine; D005444:Flunarizine; D002118:Calcium