Special Issue "Calcium Antagonists"

Guest Editor
Prof. Dr. Toni Schneider
Institute of Neurophysiology, Medical Faculty, University of Cologne, 39 50931 Köln, Germany
Website: http://www.uni-koeln.de/med-fak/physiologie/np/np_en/schneider.htm
E-Mail: Toni.Schneider@uni-koeln.de
Interests: channelopathies; “pharmacoresistant” (R-type) calcium channel

Guest Editor
Dr. Gary J. Stephens
School of Pharmacy, University of Reading, Whiteknights, PO Box 228, Reading RG6 6AJ, UK
Website: http://www.reading.ac.uk/pharmacy/about/staff/g-j-stephens.aspx
E-Mail: g.j.stephens@reading.ac.uk
Interests: SUMOylation of calcium channels; cannabinoid CB1 receptor signalling in the CNS; molecular determinants for G protein inhibition of calcium channels

Dear Colleagues,

"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 [1]. 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.

Reference List:
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
Guest Editors

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• voltage-gated calcium channels
• dihydropyridines
• phenylalkylamines
• benzothiazepines
• peptide toxins
• cloning
• crystallization