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Published ahead of print on May 19, 2004, doi:10.1165/rcmb.2003-0386OC

Am. J. Respir. Cell Mol. Biol., Volume 31, Number 3, September 2004, 337-343

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Submitted on October 29, 2003
Revised on May 19, 2004

Sub-acute hypoxia decreases Kv channel expression and function in pulmonary artery myocytes

Zhigang Hong1, E. Kenneth Weir1, Daniel P Nelson1, and Andrea Olschewski2*

1 VA Medical Center, Minneapolis, Minnesota, USA, 2 Department of Anesthesiology, Justus-Liebig-University, Giessen, Germany

* To whom correspondence should be addressed. E-mail: andrea.j.olschewski{at}physiology.med.uni-giessen.de.

Chronic hypoxia results in both structural changes in the pulmonary artery and a sustained increase in pulmonary vascular tone. This study investigated the effects of sub-acute moderate hypoxia on expression and function of potassium (K+) channels in rat pulmonary artery myocytes (PASMCs). The rats were kept at 0.67 atmospheres for 6h, 12h or 24h. We found that the expression of mRNA for voltage-activated K+ channels (Kv)1.2, Kv1.5 and Kv2.1 is reduced after less than 24 hours of this moderate hypoxia. K+ current is significantly inhibited in PASMCs from rats hypoxic for 24 hours, resting membrane potential is depolarized and cytosolic [Ca2+] is increased in these cells. In addition, antibodies to Kv1.2, Kv1.5 and Kv2.1 inhibit K+ current, cause membrane depolarization and attenuate both hypoxia- and 4-AP-induced elevation in [Ca2+]i in PASMCs from normoxic rats but not from 24 hours hypoxic rats. Sub-acute hypoxia does not completely remove the mRNA for Kv1.2, 1.5 and 2.1 but antibodies against these chances no longer alter K+ current or cytosolic calcium, suggesting that sub-acute hypoxia may inactivate the channels, as well as reducing expression. As the expression of mRNA for Kv1.2, Kv1.5 and Kv2.1 is sensitive to sub-acute hypoxia and decreased expression/function of these channels has physiologic effects on membrane potential and cytosolic calcium, it seems likely that these Kv channels may also be involved in the mechanism of high altitude pulmonary edema and possibly in the signaling of chronic hypoxic pulmonary hypertension.




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