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Adv Exp Med Biol. 2010;661:459-73. doi: 10.1007/978-1-60761-500-2_30.

Targeting TASK-1 channels as a therapeutic approach.

Author information

1
University Clinic of Anesthesia and Intensive Care Medicine, Medical University of Graz, Auenbruggerplatz 29, A-8036, Graz, Austria. andrea.olschewski@meduni-graz.at

Abstract

The voltage-independent background two-pore domain K(+) channel TASK-1 sets the resting membrane potential in excitable cells and renders these cells sensitive to a variety of vasoactive factors. There is clear evidence for TASK-1 in human pulmonary artery smooth muscle cells and TASK-1 channels are likely to regulate the pulmonary vascular tone through their regulation by hypoxia, pH, inhaled anesthetics, and G protein-coupled pathways. Furthermore, TASK-1 is a strong candidate to play a role in hypoxic pulmonary vasoconstriction. On the other hand, consistent with the activation of TASK-1 channels by volatile anesthetics, TASK-1 contributes to the anesthetic-induced pulmonary vasodilation. TASK-1 channels are unique among K(+) channels because they are regulated by both, increases and decreases from physiological pH, thus contributing to their protective effect on the pulmonary arteries. Moreover, TASK-1 may also have a critical role in mediating the vasoactive response of G protein-coupled pathways in resistance arteries which can offer promising therapeutic solutions to target diseases of the pulmonary circulation.

PMID:
20204749
DOI:
10.1007/978-1-60761-500-2_30
[Indexed for MEDLINE]
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