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Am J Physiol Heart Circ Physiol 284: H480-H490, 2003. First published October 24, 2002; doi:10.1152/ajpheart.00493.2002
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Vol. 284, Issue 2, H480-H490, February 2003

Alterations in ET-1, not nitric oxide, in 1-week-old lambs with increased pulmonary blood flow

Boaz Ovadia1, Olaf Reinhartz2, Robert Fitzgerald1, Janine M. Bekker1, Michael J. Johengen1, Anthony Azakie2, Stephan Thelitz2, Stephen M. Black3, and Jeffrey R. Fineman1,4

Departments of 1 Pediatrics and 2 Cardiothoracic Surgery, University of California, San Francisco, 94143; 3 Department of Pediatrics, Northwestern University, Chicago, Illinois 60611; and 4 Cardiovascular Research Institute, San Francisco, California 94143

Altered pulmonary vascular reactivity is a source of morbidity and mortality for children with congenital heart disease and increased pulmonary blood flow. Nitric oxide (NO) and endothelin (ET)-1 are important mediators of pulmonary vascular reactivity. We hypothesize that early alterations in endothelial function contribute to the altered vascular reactivity associated with congenital heart disease. The objective of this study was to characterize endothelial function in our lamb model of increased pulmonary blood flow at 1 wk of life. Eleven fetal lambs underwent in utero placement of an aortopulmonary vascular graft (shunt) and were studied 7 days after delivery. The pulmonary vasodilator response to both intravenous ACh (endothelium dependent) and inhaled NO (endothelium independent) was similar in shunted and control lambs. In addition, tissue NOx, NO synthase (NOS) activity, and endothelial NOS protein levels were similar. Conversely, the vasodilator response to both ET-1 and 4Ala-ET-1 (an ETB receptor agonist) were attenuated in shunted lambs, and tissue ET-1 concentrations were increased (P < 0.05). Associated with these changes were an increase in ET-converting enzyme-1 protein and a decrease in ETB receptor protein levels (P < 0.05). These data demonstrate that increased pulmonary blood flow induces alterations in ET-1 signaling before NO signaling and suggest an early role for ET-1 in the altered vascular reactivity associated with increased pulmonary blood flow.

endothelin; pulmonary hypertension; pulmonary circulation


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