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Articles in PresS, published online ahead of print June 5, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00475.2001
Submitted on December 13, 2001
Accepted on May 30, 2002
1 Division of Pulmonary and critical care Medicine, Rhode Isalnd Hospital, Brown University School of Medicine, Providence, RI, USA
2 Division of Pulmonary and critical care Medicine, Rhode Isalnd Hospital, Brown University School of Medicine, Providence, RI, USA; Veterans Administration Medical Center, Providence, RI, USA
* To whom correspondence should be addressed. E-mail: mkaramsetty{at}lifespan.org.
Mitogen activated protein (MAP) kinases regulate smooth muscle cell contraction. Hypoxia contracts pulmonary arteries by mechanisms that are incompletely understood. We hypothesized that hypoxic contraction of pulmonary arteries involves activation of the MAP kinases. To test this hypothesis, we studied the effects of SB202190, a p38 MAP kinase inhibitor, PD98059 and UO126, two structurally different MEKK inhibitors and anisomycin, a stimulator of p38 MAP kinase on acute hypoxia-induced contraction in rat conduit pulmonary artery rings pre-contracted with phenylephrine or KCl. Hypoxia induced a transient contraction, followed by a relaxation, and then a slowly developing sustained contraction. Hypoxia also significantly increased phosphorylation of p38 MAP kinase. SB202190 did not affect the transient phase but abrogated the sustained phase of hypoxic contraction, whereas anisomycin enhanced both phases of contraction. SB202190 also attenuated and anisomycin enhanced the phenylephrine-induced contraction. In contrast, PD98059 and UO126 had minimal effects on either hypoxic or phenylephrine-induced contraction. None of the treatments modified KCl-induced contraction. We conclude that p38, but not the ERK1/ERK2 MAP kinase pathway, mediates the sustained phase of hypoxic contraction in isolated rat pulmonary arteries.
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