Nitric oxide in the pulmonary vasculature

Coggins, Matthew P.; Bloch, Kenneth D.

doi:10.1161/atvbaha.107.142943

Cited by 138Nitric Oxide and Endothelin EffectsPulmonary Hypertension Research and TreatmentsCardiovascular Health and Disease Prevention

Nitric oxide in the pulmonary vasculature

Coggins, Matthew P., Bloch, Kenneth D.·2007·Arteriosclerosis Thrombosis and Vascular Biology

DOI 10.1161/atvbaha.107.142943

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Abstract

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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The majority of NO is derived from the oxidation of L-arginine by three isoforms of nitric oxide synthase (NOS) in a reaction requiring oxygen, NADPH, tetrahydrobiopterin (BH4) and other cofactors.
“Classically, the majority of NO is derived from the oxidation of the essential amino acid, L-arginine by a set of 3 isoforms of the enzyme nitric oxide synthase (NOS) in a reaction requiring oxygen, reduced nicotinamide-adenine dinucleotide phosphate (NADPH), tetrahydrobiopterin (BH4) and other cofactors[20,22].”
From Enterosalivary nitrate metabolism and the microbiome: Intersection of microbial metabolism, nitric oxide and diet in cardiac and pulmonary vascular health (2017) · cites this paper as [22]

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Authors: Coggins, M. P., & Bloch, K. D.
Affiliations: Massachusetts General Hospital (US)
Venue: Arteriosclerosis Thrombosis and Vascular Biology
Publisher: Ovid Technologies (Wolters Kluwer Health)
Published: 2007-09
Volume: 27
Issue: 9
Pages: 1877-1885
ISSN: 1079-5642 (ISSN-L)
1524-4636
DOI: 10.1161/atvbaha.107.142943
OpenAlex: W2130449101
Cited by: 138
References: 116
Citations by year: 2026: 1 · 2025: 2 · 2024: 2 · 2023: 7 · 2022: 5 · 2021: 3 · 2020: 2 · 2019: 2 · 2018: 3 · 2017: 7 · 2016: 5 · 2015: 7 · 2014: 14 · 2013: 8 · 2012: 18
FWCI: 1.43
Type: journal article
Language: en
Open access: closed
Locations: Arteriosclerosis Thrombosis and Vascular Biology (publishedVersion)
PubMed (publishedVersion)
Topics: Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Pulmonary Hypertension Research and Treatments
Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Health and Disease Prevention
Keywords: nitric oxide, pulmonary vasculature, pulmonary hypertension, endothelial dysfunction, NO bioavailability, vascular regulation, no-signaling, inhaled nitric oxide, phosphodiesterase inhibitors, nitric oxide donors, soluble guanylate cyclase, nitric oxide synthase, progenitor cells
MeSH terms: Animals, Homeostasis, Humans, Hypertension, Pulmonary, Nitric Oxide, Pulmonary Circulation, Signal Transduction, Mice, Rats

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Nitric oxide in the pulmonary vasculature

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