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Acta Physiol (Oxf). 2009 Feb;195(2):247-58. doi: 10.1111/j.1748-1716.2008.01884.x. Epub 2008 Jul 30.

Purinergic activation of a leak potassium current in freshly dissociated myocytes from mouse thoracic aorta.

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Department of Zoology and Animal Biology, University of Geneva, Sciences III, Geneva, Switzerland.



Exogenous ATP elicits a delayed calcium-independent K(+) current on freshly isolated mouse thoracic aorta myocytes. We investigated the receptor, the intracellular pathway and the nature of this current.


The patch-clamp technique was used to record ATP-elicited delayed K(+) current in freshly dissociated myocytes.


ATP-elicited delayed K(+) current was not inhibited by a 'cocktail' of K(+) channel blockers (4-AP, TEA, apamin, charybdotoxin, glibenclamide). The amplitude of the delayed K(+) current decreased after the reduction of extracellular pH from 7.4 to 6.5. These two characteristics suggest that this current could be carried by the TASK subfamily of 'twin-pore potassium channels' (K2P). Purinergic agonists including dATP, but not ADP, activated the delayed K(+) current, indicating that P2Y(11) is the likely receptor involved in its activation. The PKC activator phorbol ester 12,13-didecanoate stimulated this current. In addition, the PKC inhibitor Gö 6850 partially inhibited it. Real-time quantitative PCR showed that the genes encoding TASK-1 and TASK-2 are expressed.


Our results indicate that blocker cocktail-insensitive delayed K(+) current in freshly dissociated aortic myocytes is probably carried by the TASK subfamily of twin-pore channels.

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