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Erschienen in: Drugs 1/2009

01.01.2009 | Leading Article

Development of Newer Calcium Channel Antagonists

Therapeutic Potential of Efonidipine in Preventing Electrical Remodelling during Atrial Fibrillation

verfasst von: Dr Narutaka Ohashi, Hideo Mitamura, Satoshi Ogawa

Erschienen in: Drugs | Ausgabe 1/2009

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Abstract

Calcium channel antagonists are most frequently prescribed for the treatment of hypertension and the majority specifically inhibit the L-type Ca2+ channel. In order to prevent reflex sympathetic over activity caused by L-type calcium channel antagonists (calcium channel blockers [CCBs]), increasing attention has focused on the blockade of the T-type Ca2+ channel. The T-type Ca2+ channel is found in the kidney and can also appear in the ventricle of the heart when in failure. Therefore, the T-type Ca2+ channel is a possible new target for the treatment of nephropathy and heart failure. In clinical trials, the efficacy and safety of T-type CCBs in hypertension and chronic renal disease have been reported.
It is well known that the T-type Ca2+ channel is present in the adult atrium and plays a role in the cardiac pacemaker, but recent experimental studies suggest that this current also promotes electrical remodelling of the atrium. Using efonidipine, a dual L- and T-type CCB, it has been demonstrated that atrial electrical remodelling can be diminished in dogs. Furthermore, the T-type Ca2+ channel has recently been found in the pulmonary veins, contributing to the pulmonary vein pacemaker activity and triggered activity. A variety of drugs having T-type CCB effects have been shown to be effective in the management of atrial fibrillation, suggesting that this channel may be a novel therapeutic target.
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Metadaten
Titel
Development of Newer Calcium Channel Antagonists
Therapeutic Potential of Efonidipine in Preventing Electrical Remodelling during Atrial Fibrillation
verfasst von
Dr Narutaka Ohashi
Hideo Mitamura
Satoshi Ogawa
Publikationsdatum
01.01.2009
Verlag
Springer International Publishing
Erschienen in
Drugs / Ausgabe 1/2009
Print ISSN: 0012-6667
Elektronische ISSN: 1179-1950
DOI
https://doi.org/10.2165/00003495-200969010-00002

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