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Articles in PresS, published online ahead of print November 14, 2001
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00417.2001
Submitted on May 17, 2001
Accepted on October 31, 2001
1 Pediatrics, University of California, San Francisco, San Francisco, CA, USA
2 Cardiothoracic Surgery, University of California, San Francisco, San Francisco, CA, USA
3 Pediatrics, New York University, New York, NY, USA
4 Pediatrics, Northwestern University, Chicago, IL, USA
5 Pediatrics, University of California, San Francisco, San Francisco, CA, USA; Cardiovascular Research Institute, University of California, San Francisco, San Francisco, CA, USA
* To whom correspondence should be addressed. E-mail: jfineman{at}pedcard.ucsf.edu.
Acute partial compression of the fetal ductus arteriosus (DA) results in an initial increase in pulmonary blood flow (PBF), which is followed by acute vasoconstriction. The objective of the present study was to determine the role of nitric oxide (NO)-endothelin-1 (ET-1) interactions in the acute changes in pulmonary vascular tone following in utero partial constriction of the DA. Twelve late gestation fetal lambs (132-140 days) were instrumented to measure vascular pressures and left PBF. After a 24 hour recovery, acute constriction of the ductus arteriosus was performed by partially inflating a vascular occluder, and the hemodynamic variables were observed for 4 hours. In control lambs (n=7), acute ductal constriction initially increased PBF by 627% (P<0.05). However, this was followed by active vasoconstriction, such that PBF was restored to pre-constriction values by 4 hours. This was associated with a 43% decrease in total NOS activity (P<0.05), and a 106% increase in plasma ET-1 levels (P<0.05). Western blot analysis demonstrated no changes in lung tissue eNOS, preproET-1, ECE-1, or ETB receptor protein levels. The infusion of PD 156707 (an ETA receptor antagonist, n=5) completely blocked the vasoconstriction, and preserved NOS activity. These data suggest that the fetal pulmonary vasoconstriction following acute constriction of the ductus arteriosus are mediated by NO-ET-1 interactions. These include an increase in ETA receptor-mediated vasoconstriction, and an ETA receptor-mediated decrease in NOS activity. The mechanisms of these NO-ET-1 interactions, and their role in mediating acute changes in PBF warrant further studies.
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