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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2007;27:1877.)
© 2007 American Heart Association, Inc.

Brief Reviews

Nitric Oxide in the Pulmonary Vasculature

Matthew P. Coggins; Kenneth D. Bloch

From the Cardiology Division of the Department of Medicine and the Department of Anesthesia and Critical Care, Massachusetts General Hospital, Boston.

Correspondence to Matthew P. Coggins, MD, Cardiology Division, Massachusetts General Hospital, 55 Fruit Street, Boston, MA 02114. E-mail mcoggins{at}partners.org

Series Editor: Joseph Loscalzo
Nitric Oxide Redux
ATVB In Focus

Previous Brief Reviews in this Series:

•Gotoh T, Mori M. Nitric oxide and endoplasmic reticulum stress. Arterioscler Thromb Vasc Biol. 2006;26:1439–1445.
•Kim-Shapiro DB, Schechter AN, Gladwin MT. Unraveling the reactions of nitric oxide, nitrite, and hemoglobin in physiology and therapeutics. Arterioscler Thromb Vasc Biol. 2006;26:1207.
•Handy DE, Loscalzo J. Nitric oxide and posttranslational modification of the vascular proteome: s-nitrosation of reactive thiols. Arterioscler Thromb Vasc Biol. 2006;26:697.
•Loscalzo J. Nitric oxide redux. Arterioscler Thromb Vasc Biol. 2006;26:696.

Homeostasis in the pulmonary vasculature is maintained by the actions of vasoactive compounds, including nitric oxide (NO). NO is critical for normal development of the pulmonary vasculature and continues to mediate normal vasoregulation in adulthood. Loss of NO bioavailability is one component of the endothelial dysfunction and vascular pathology found in pulmonary hypertension (PH). A broad research effort continues to expand our understanding of the control of NO production and NO signaling and has generated novel theories on the importance of pulmonary NO production in the control of the systemic vasculature. This understanding has led to exciting developments in our ability to treat PH, including inhaled NO and phosphodiesterase inhibitors, and to several promising directions for future therapies using nitric oxide-donor compounds, stimulators of soluble guanylate cyclase, progenitor cells expressing NO synthase (NOS), and NOS gene manipulation.

Loss of nitric oxide (NO) bioavailability is one component of the endothelial dysfunction and vascular pathology found in pulmonary hypertension (PH). Our understanding of the control of NO production and NO signaling continues to grow. This understanding has led to developments in the treatment of PH and to promising directions for future therapies.

Key Words: nitric oxide • pulmonary vasculature • pulmonary hypertension treatment

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