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Articles in PresS, published online ahead of print April 5, 2002
J Appl Physiol, 10.1152/jap.01083.2001
Submitted on October 30, 2001
Accepted on March 27, 2002
1 Department of Pediatrics, University of New Mexico, Albuquerque, New Mexico, USA; Departments of Cell Biology and Physiology, University of New Mexico, Albuquerque, New Mexico, USA
2 Department of Pediatrics, University of New Mexico, Albuquerque, New Mexico, USA
3 Departments of Cell Biology and Physiology, University of New Mexico, Albuquerque, New Mexico, USA
* To whom correspondence should be addressed. E-mail: lchicoine{at}salud.unm.edu.
Chronic hypoxia (CH) increases pulmonary endothelial nitric oxide synthase (eNOS) protein levels in adult rats, but decreases eNOS protein levels in neonatal pigs. We hypothesized that this differing response to CH is due to developmental rather than species differences. Adult and neonatal rats were placed in either hypobaric-hypoxia or normoxia for 14 days. At that time, body weight (BW), hematocrit (Hct), plasma nitrite/nitrate (NOx-), right ventricular (RV) and total ventricular (T) heart weights were measured. Percent pulmonary artery wall area (% wall area) of 20-50 µm and 51-100 µm arteries were also determined. Total lung protein extracts were assayed for eNOS levels using immune-blot analysis. Compared to their respective normoxic controls, both adult and neonatal hypoxic groups demonstrated significantly decreased BW, elevated Hct, and elevated RV/T ratios. Both, adult and neonatal hypoxic groups also demonstrated significantly larger % wall area compared to their respective normoxic controls. Hypoxic adult pulmonary eNOS protein and plasma NOx- were significantly greater than levels found in normoxic adults. In contrast, hypoxic neonatal pulmonary eNOS protein and plasma NOx- were significantly less compared to normoxic neonates. We conclude that there is a developmental difference in eNOS expression and NO production in response to CH.
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