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MINIREVIEW
Nitric Oxide Synthase in Pulmonary Hypertension: Lessons from Knockout Mice
K. A. Fagan1,2, I. McMurtry1,2,
D. M. Rodman1,2,3
1Division of Pulmonary Sciences and Critical Care Medicine, 2Cardiovascular
Pulmonary Research Laboratory, and 3Department of Physiology,
University of Colorado Health Sciences Center, Denver, USA
Received February 29, 2000
Accepted April 3, 2000
Summary
Nitric oxide (NO) is implicated in a wide variety of
biological roles. NO is generated from three nitric oxide synthase (NOS)
isoforms: neuronal (nNOS), inducible (iNOS), and endothelial (eNOS) all of which
are found in the lung. While there are no isoform-specific inhibitors of NOS,
the recent development and characterization of mice deficient in each of the NOS
isoforms has allowed for more comprehensive study of the importance of NO in the
lung circulation. Studies in the mouse have identified the role of NO from eNOS
in modulating pulmonary vascular tone and in attenuating the development of
chronic hypoxic pulmonary hypertension.
Key words
Nitric oxide ● Knockout mice ● Pulmonary hypertension ●
Pulmonary vasoreactivity ● Vascular remodeling
Reprint requests
Karen A. Fagan, MD, University of Colorado Health Sciences
Center, 4200 East Ninth Ave. B-133, Denver, CO 80262, USA. Email: karen.fagan@uchsc.edu
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