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This Article Full Text Full Text (PDF) All Versions of this Article: 291/6/L1169    most recent 00117.2006v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Fike, C. D. Articles by Madden, J. A. Search for Related Content PubMed PubMed Citation Articles by Fike, C. D. Articles by Madden, J. A.

Voltage-gated K⁺ channels at an early stage of chronic hypoxia-induced pulmonary hypertension in newborn piglets

Department of Neurology, Medical College of Wisconsin, Milwaukee, Wisconsin; Department of Pediatrics, Vanderbilt University School of Medicine, Nashville, Tennessee; and Department of Pediatrics, Wake Forest University School of Medicine, Winston-Salem, North Carolina

Submitted 29 March 2006 ; accepted in final form 27 June 2006

Our purpose was to determine whether smooth muscle cell membrane properties are altered in small pulmonary arteries (SPA) of piglets at an early stage of pulmonary hypertension. Piglets were raised in either room air (control) or hypoxia for 3 days. A microelectrode technique was used to measure smooth muscle cell membrane potential (E_m) in cannulated, pressurized SPA (100- to 300-µm diameter). SPA responses to the voltage-gated K⁺ (K_V) channel antagonist 4-aminopyridine (4-AP) and the K_V1 family channel antagonist correolide were measured. Other SPA were used to assess amounts of K_V1.2, K_V1.5, and K_V2.1 (immunoblot technique). E_m was more positive in SPA of chronically hypoxic piglets than in SPA of comparable-age control piglets. The magnitude of constriction elicited by either 4-AP or correolide was diminished in SPA from hypoxic piglets. Abundances of K_V1.2 were reduced, whereas abundances of both K_V1.5 and K_V2.1 were unaltered, in SPA from hypoxic piglets. At least partly because of reduced amounts of K_V1.2, smooth muscle cell membrane properties are altered such that E_m is depolarized and K_V channel family function is impaired in SPA of piglets at an early stage of chronic hypoxia-induced pulmonary hypertension.

membrane potential; membrane depolarization; K_V1.2; K_V1.5; K_V2.1; 4-aminopyridine; correolide