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1 Department of Pediatrics, Wake Forest University School of Medicine, Winston-Salem, NC, USA
* To whom correspondence should be addressed. E-mail: cfike{at}wfubmc.edu.
We performed studies to determine whether chronic hypoxia impairs NO signaling in resistance level pulmonary arteries (PAs) of newborn piglets. Piglets were maintained in room air (control) or hypoxia (11% O2) for either 3 (shorter exposure) or 10 (longer exposure) days. Responses of PAs to a nonselective NOS antagonist, Nwnitro-larginine methylester (L-NAME), a NOS 2 selective antagonist, aminoguanidine (AG), and a NOS 1 selective antagonist, 7-nitroindazole (7-NINA) were measured. Levels of NOS isoforms and of two proteins involved in NOS signaling, heat shock protein 90 (Hsp90) and caveolin-1, were assessed in PA homogenates. PAs from all groups constricted to L-NAME but not to AG nor to 7-NINA. The magnitude of constriction to L-NAME was similar for PAs from control and hypoxic piglets of the shorter exposure period but was diminished for PAs from hypoxic as compared to control piglets of the longer exposure period. NOS 3, Hsp90, and caveolin-1 levels were similar in hypoxic and control PAs. These findings indicate that NOS 3, but not NOS 2 nor NOS 1, is involved with basal NO production in PAs from both control and hypoxic piglets. After 10 days of hypoxia, NO function is impaired in PAs despite preserved levels of NOS 3, Hsp90 and caveolin-1. The development of NOS 3 dysfunction in resistance level pulmonary arteries may contribute to the progression of chronic hypoxia-induced pulmonary hypertension in newborn piglets.
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