Special Issue "Calcium Antagonists"

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A special issue of Pharmaceuticals (ISSN 1424-8247).

Deadline for manuscript submissions: closed (28 February 2013)

Special Issue Editors

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

Special Issue Information

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

Submission

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. Papers will be published continuously (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are refereed through a peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Pharmaceuticals is an international peer-reviewed Open Access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 800 CHF (Swiss Francs).

Keywords

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

Published Papers (5 papers)

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Displaying article 1-5
p. 788-812
by , ,  and
Pharmaceuticals 2013, 6(7), 788-812; doi:10.3390/ph6070788
Received: 29 March 2013; in revised form: 6 June 2013 / Accepted: 6 June 2013 / Published: 26 June 2013
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(This article belongs to the Special Issue Calcium Antagonists)
p. 777-787
by , ,  and
Pharmaceuticals 2013, 6(6), 777-787; doi:10.3390/ph6060777
Received: 25 February 2013; in revised form: 13 May 2013 / Accepted: 14 May 2013 / Published: 29 May 2013
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(This article belongs to the Special Issue Calcium Antagonists)
p. 689-699
by  and
Pharmaceuticals 2013, 6(6), 689-699; doi:10.3390/ph6060689
Received: 4 March 2013; in revised form: 15 April 2013 / Accepted: 2 May 2013 / Published: 23 May 2013
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(This article belongs to the Special Issue Calcium Antagonists)
p. 623-633
by , , , , ,  and
Pharmaceuticals 2013, 6(5), 623-633; doi:10.3390/ph6050623
Received: 21 December 2012; Accepted: 19 April 2013 / Published: 29 April 2013
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(This article belongs to the Special Issue Calcium Antagonists)
p. 70-84
by ,  and
Pharmaceuticals 2013, 6(1), 70-84; doi:10.3390/ph6010070
Received: 11 December 2012; in revised form: 28 December 2012 / Accepted: 11 January 2013 / Published: 15 January 2013
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Last update: 9 October 2012

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