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Am J Physiol Lung Cell Mol Physiol (February 15, 2002). doi:10.1152/ajplung.00004.2002
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Articles in PresS, published online ahead of print February 15, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00004.2002
Submitted on January 7, 2002
Accepted on February 14, 2002

Chronic carbon monoxide enhanced IbTx-sensitive currents in rat resistance pulmonary artery smooth muscle cells

Eric Dubuis1, Mathieu Gautier1, Alexandre Melin1, Manuel Rebocho1, Catherine Girardin1, Pierre Bonnet1, and Christophe Vandier1*

1 Faculte de Medecine, Laboratoire de Physiopathologie de la Paroi Arterielle, TOURS, France

* To whom correspondence should be addressed. E-mail: vandier{at}univ-tours.fr.

Exogenous carbon monoxide (CO) can induce pulmonary vasodilation by acting directly on pulmonary artery (PA) smooth muscle cells. We investigated the contribution of K+ channels to the regulation of resistance PA resting membrane potential on control (PAC) rats and rats exposed to CO for 3 weeks at 530 p.p.m labeled as (PACO) rats.Whole-cell patch-clamp experiment revealed that resting membrane potential of PACO cells was more negative than that of PAC cells. This was associated with a decrease of membrane resistance in PACO cells. Additional analysis showed that outward current-density in PACO cells was higher (50 % at +60mV) than in PAC cells. This was linked to an increase of iberiotoxin (IbTx)-sensitive current. Chronic CO hyperpolarized membrane of pressurized PA from -46.9 ± 1.2mV to -56.4 ± 2.6mV. Additionally, IbTx significantly depolarized membrane of smooth muscle cells from PACO arteries but not from PAC arteries. The present study provides initial evidence of an increase of KCa current in smooth muscle cells from PA of rats exposed to chronic CO.




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