Special Issue "Calcium Antagonists"
A special issue of Pharmaceuticals (ISSN 1424-8247).
Deadline for manuscript submissions: closed (28 February 2013)
"Calcium antagonism“ was initially developed as a novel pharmacodynamic concept, which prevented cytosolic Ca2+ increase in cardiac tissue. It was initially developed by the A. Fleckenstein group in Freiburg . The therapeutic consequences are widespread and are initiated by the inhibition of the transmembrane Ca2+ flux. Such an antagonism normalizes hyperkinetic cardiac disorders, suppresses arterial and arteriolar spasms, relieves systemic arterial hypertension and may stop cardiac arrhythmia.
Initially, the targets of classical Ca2+ channel antagonists were only named as “receptors” as Ca2+ channels proteins underlying these responses remained unidentified. Subsequently, ten different genes were successfully cloned for the voltage-gated ion conducting pore, and an increasing number of auxiliary or interacting subunits were identified.
Ca2+ channel antagonists were instrumental in the determination of function for each of the voltage-gated Ca2+ channels. In the genomic age, the development of mouse models with gene inactivated subunits has significantly aid the deduction of their function. The molecular interaction of Ca2+ channel subunits was and will be specified by high resolution crystallography. We now also have some information about the Ca2+ channel proteome. Knowing the molecular minimal structure for interactions will also accelerate the development of more selective Ca2+ channel antagonists. Novel powerful compounds are needed, because some Ca2+ channels are still lacking selective antagonism including the “resistant” (R-) type, and the T-type voltage-gated Ca2+ channels.
1. Fleckenstein A. Historical overview. The calcium channel of the heart. Ann. N.Y. Acad. Sci. 1988, 522, 1-15.
Prof. Dr. Toni Schneider
Dr. Gary J. Stephens
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- voltage-gated calcium channels
- peptide toxins