Perspectives: The Ca2+-dependent K+-channel K Ca3.1 as a therapeutic target in cardiovascular disease

Rainer Windler, Cor De Wit*

*Korrespondierende/r Autor/-in für diese Arbeit
2 Zitate (Scopus)


The endothelium is an interesting target to modify cardiovascular disease. In addition to the well-known autacoids such as nitric oxide and prostaglandins, a third endothelial pathway exists which relaxes vascular smooth muscle through hyperpolarization (endothelium-dependent hyperpolarization-type dilation). Herein, calcium-activated potassium channels (KCa) are crucial in which two types are expressed in endothelial cells (KCa3.1, K Ca2.3). Specifically, KCa3.1 is selectively activated by small molecules that are potentially useful as pharmacological compounds which lead to overall vascular dilation including the coronary bed and a decrease in arterial pressure. Conversely, blockade of this channel reduces atherosclerosis and neointima formation since under these conditions KCa3.1 is up-regulated in phenotypically modulated, proliferative smooth muscle cells and supports migration and proliferation. This review briefly summarizes main experimental findings on this channel.

ZeitschriftEuropean Heart Journal, Supplement
Seiten (von - bis)A30-A32
PublikationsstatusVeröffentlicht - 01.2014

Strategische Forschungsbereiche und Zentren

  • Forschungsschwerpunkt: Gehirn, Hormone, Verhalten - Center for Brain, Behavior and Metabolism (CBBM)


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