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Am J Physiol Heart Circ Physiol 280: H777-H785, 2001;
0363-6135/01 $5.00
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Vol. 280, Issue 2, H777-H785, February 2001

Inhaled nitric oxide-induced rebound pulmonary hypertension: role for endothelin-1

D. Michael McMullan1, Janine M. Bekker2, Michael J. Johengen2, Karen Hendricks-Munoz4, Rene Gerrets4, Stephen M. Black5, and Jeffrey R. Fineman2,3

1 Department of Cardiothoracic Surgery and 2 Department of Pediatrics and 3 Cardiovascular Research Institute, University of California, San Francisco, San Francisco, California 94143-0106; 4 Department of Pediatrics, New York University, New York, New York 10016; and 5 Department of Pediatrics, Northwestern University Medical School, Chicago, Illinois 60611

Clinically significant increases in pulmonary vascular resistance have been noted on acute withdrawal of inhaled nitric oxide (NO). Endothelin (ET)-1 is a vasoactive peptide produced by the vascular endothelium that may participate in the pathophysiology of pulmonary hypertension. The objectives of this study were to determine the effects of inhaled NO on endogenous ET-1 production in vivo in the intact lamb and to determine the potential role of ET-1 in the rebound pulmonary hypertension associated with the withdrawal of inhaled NO. Seven 1-mo-old vehicle-treated control lambs and six PD-156707 (an ETA receptor antagonist)-treated lambs were mechanically ventilated. Inhaled NO (40 parts per million) was administered for 24 h and then acutely withdrawn. After 24 h of inhaled NO, plasma ET-1 levels increased by 119.5 ± 42.2% (P < 0.05). Western blot analysis revealed that protein levels of preproET-1, endothelin-converting enzyme-1alpha , and ETA and ETB receptors were unchanged. On acute withdrawal of NO, pulmonary vascular resistance (PVR) increased by 77.8% (P < 0.05) in control lambs but was unchanged (-5.5%) in PD-156707-treated lambs. Inhaled NO increased plasma ET-1 concentrations but not gene expression in the intact lamb, and ETA receptor blockade prevented the increase in PVR after NO withdrawal. These data suggest a role for ET-1 in the rebound pulmonary hypertension noted on acute withdrawal of inhaled NO.

endothelium-derived factors; pulmonary heart disease; endothelin receptor; pulmonary hypertension of the newborn


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