Key result
Nitric oxide is critical for pulmonary vasoregulation, and its reduced bioavailability in pulmonary hypertension has driven the development of targeted therapies like inhaled NO and PDE inhibitors.
Nitric oxide plays a critical role in pulmonary vascular homeostasis, and targeting its pathway remains a key strategy for treating pulmonary hypertension.
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.
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Coggins et al. (2007) conducted a review in Pulmonary hypertension. Nitric oxide and related therapies was evaluated. Nitric oxide is critical for pulmonary vasoregulation, and its reduced bioavailability in pulmonary hypertension has driven the development of targeted therapies like inhaled NO and PDE inhibitors.
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