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Articles in PresS, published online ahead of print March 28, 2002
Am J Physiol Regu Physiol, 10.1152/ajpregu.00741.2001
Submitted on December 17, 2001
Accepted on December 31, 1969
1 Deparment of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin, USA
2 Department of Biochemistry, University of Texas Southwestern Medical Center, Dallas, Texas, USA
* To whom correspondence should be addressed. E-mail: jfrisbee{at}mcw.edu.
Mediator contributions to hypoxic dilation of rat gracilis muscle resistance arteries were determined by measuring dilation, vascular smooth muscle hyperpolarization and metabolite production following incremental hypoxia. Nitric oxide (NO) synthase inhibition abolished responses to mild hypoxia, while cyclooxygenase (COX) inhibition impaired responses to more severe hypoxia by 77%. Blocking 20-HETE impaired responses to moderate hypoxia. With only NO systems intact, responses were maintained with mild hypoxia (88% normal); mediated via KCa channels. When only COX pathways were intact, responses to moderate-severe hypoxia were largely retained (79% of normal); mediated via KATP channels. Vessel responses to moderate hypoxia were retained with only 20-HETE systems intact, mediated via KCa channels. NO production increased 5.6-fold with mild hypoxia; greater hypoxia was without further effect. With increased hypoxia, 20-HETE levels fell to 40% of control values. 6-keto-PGF1
levels were not altered with mild hypoxia, but increased 4.6-fold with severe hypoxia. These results suggest vascular reactivity to progressive hypoxia represents an integration of NO production (mild hypoxia), PGI2 production (severe hypoxia) and reduced 20-HETE levels (moderate hypoxia).
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