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Laboratoire de Physiopathologie de la Paroi Artérielle, Faculté de Médecine, 37032 Tours, France
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 wk at 530 parts/million, labeled as PACO rats.
Whole cell patch-clamp experiments revealed that the 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 +60 mV) 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 ± 1.2 to
56.4 ± 2.6 mV. 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
Ca2+-activated K+ current in smooth muscle
cells from PA of rats exposed to chronic CO.
Kv; K channel blockers; 4-aminopyridine; pressurized artery; iberiotoxin
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