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Cardiovascular Research 2005 68(1):5-7; doi:10.1016/j.cardiores.2005.07.018
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Copyright © 2005, European Society of Cardiology

Non-capacitative calcium entry–Extension of the possibilities for calcium entry in vascular tissue

Rudolf Schubert*

University of Rostock, Institute of Physiology, PSF 100888, D-18055 Rostock, Germany

* Corresponding author. Tel.: +49 381 4948016; fax: +49 381 4948002. Email address: rudolf.schubert@medizin.uni-rostock.de

Received 18 July 2005; accepted 25 July 2005

The first 10% of the full text of this article appears below.

See article by Thomas et al. [5] (pages 56–64) in this issue.

The functional state of blood vessels is regulated by the calcium sensitivity of the contractile elements and the intracellular calcium concentration. The latter is determined by the balance between the activity of calcium sources (influx from the extracellular space and release from intracellular stores), the activity of calcium sinks (extrusion to the extracellular space and sequestration into intracellular stores), and the capacity of calcium buffers. Contractile reactions of blood vessels are depressed considerably after removal of extracellular calcium ions, emphasizing the importance of calcium entry for vessel contractility. Classically, voltage-operated calcium influx via L-type calcium channels had been assigned a leading role in calcium entry. However, a considerable number . . . [Full Text of this Article]


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