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Vol. 300, Issue 3, 724-728, March 2002
Section on Molecular and Clinical Pharmacology, Laboratory of
Clinical Investigation, National Institute on Aging, Intramural
Research Program, National Institutes of Health, Baltimore, Maryland
The L-type Ca2+ channels mediate depolarization-induced
influx of Ca2+ into a wide variety of cells and thus play a
central role in triggering cardiac and smooth muscle contraction.
Because of this role, clinically important classes of
1,4-dihydropyridine, phenylalkylamine, and benzothiazepine
Ca2+ channel blockers were developed as powerful medicines
to treat hypertension and angina pectoris. Molecular cloning studies
revealed that the channel is subject to extensive structure-functional variability due to alternative splicing. In this review, we will focus
on a potentially important role of genetically driven variability of
Ca2+ channels in expression regulation and mutations,
Ca2+-induced inactivation, and modulation of sensitivity to
Ca2+ channel blockers with the perspective for new
pharmacological targets.
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