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Articles in PresS, published online ahead of print November 9, 2001
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00272.2001
Submitted on July 19, 2001
Accepted on October 22, 2001
1 Pediatrics, University of Colorado, Denver, CO, USA
2 Howard Hughes Medical Institute, University of Texas Southwestern, Dallas, TX, USA
3 Medicine / CVP, University of Colorado, Denver, CO, USA
* To whom correspondence should be addressed. E-mail: dunbar.ivy{at}UCHSC.edu.
Mechanisms by which ET-1 mediates chronic pulmonary hypertension remain incompletely understood. Although activation of the ETA receptor causes vasoconstriction, stimulation of ETB receptors can elicit either vasodilation or vasoconstriction. We hypothesized that the ETB receptor attenuates the development of hypoxic pulmonary hypertension and studied a genetic rat model of ETB receptor deficiency (transgenic sl/sl). After 3 weeks of severe hypoxia, the transgenic sl/sl pulmonary vasculature lacked expression of mRNA for the ETB receptor and developed exaggerated pulmonary hypertension that was characterized by elevated pulmonary artery pressure, diminished cardiac output, and increased total pulmonary resistance. Plasma ET-1 was five-fold higher in transgenic sl/sl rats than in transgenic controls. Although mRNA for preproendothelin-1 was not different, mRNA for endothelin converting enzyme-1 was higher in transgenic sl/sl lungs than in transgenic control lungs. Hypertensive lungs of sl/sl rats also produced less NOx, nitric oxide metabolites, and 6 keto-PGF1
, a metabolite of prostacyclin, than those of transgenic controls. These findings suggest that the ETB receptor plays a protective role in the pulmonary hypertensive response to chronic hypoxia.
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