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Vascular System: Role of Nitric Oxide in Cardiovascular Diseases
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In contrast with the short research history of the enzymatic synthesis of nitric oxide (NO), the introduction of nitrate-containing compounds for medicinal purposes marked its 150th anniversary in 1997. Glyceryl trinitrate (nitroglycerin) is the first compound of this category. On October 12, 1998, the Nobel Assembly awarded the Nobel Prize in Medicine or Physiology to scientists Robert Furchgott, Louis Ignarro, and Ferid Murad for their discoveries concerning NO as a signaling molecule in the cardiovascular system. NO-mediated signaling is a recognized component in various physiologic processes (eg, smooth muscle relaxation, inhibition of platelet and leukocyte aggregation, attenuation of vascular smooth muscle cell proliferation, neurotransmission, and immune defense), to name only a few. NO has also been implicated in the pathology of many inflammatory diseases, including arthritis, myocarditis, colitis, and nephritis and a large number of pathologic conditions such as amyotrophic lateral sclerosis, cancer, diabetes, and neurodegenerative diseases. Some of these processes (eg, smooth muscle relaxation, platelet aggregation, and neurotransmission) require only a brief production of NO at low nanomolar concentrations and are dependent on the recruitment of cyclic guanosine monophosphate (cGMP)-dependent signaling. Other processes are associated with direct interaction of NO or reactive nitrogen species derived from it with target proteins and requires a more sustained production of NO at higher concentrations but do not involve the cGMP pathway.
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“It is well known that endothelium-derived nitric oxide (NO) plays an important role in vascular homeostasis and cardiac function based on seminal studies leading to the Nobel Prize in Physiology or Medicine in 1998 [9, 10].”
From Inorganic nitrite therapy: historical perspective and future directions (2011) · cites this paper as [9]
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Sirek, N. (2013) · Turkish Journal of Thoracic and Cardiovascular Surgery · doi:10.5606/tgkdc.dergisi.2013.7753 · Cited by 1
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Metadata
- Authors
- Bian, K., Doursout, M., & Murad, F.
- Affiliations
- The University of Texas Health Science Center at Houston (US)
- Corresponding author
- Murad, Ferid
- Venue
- The Journal of Clinical Hypertension
- Publisher
- Wiley
- Published
- 2008-04
- Volume
- 10
- Issue
- 4
- Pages
- 304-310
- ISSN
- 1524-6175 (ISSN-L)
- 1751-7176
- PMC
- PMC8109995
- OpenAlex
- W2004742560
- Semantic Scholar
- 3f0ea8307ce77731d0e60b1fcc78d664629064bb
- Cited by
- 229
- References
- 41
- Citations by year
- 2026: 8 · 2025: 5 · 2024: 10 · 2023: 10 · 2022: 8 · 2021: 13 · 2020: 9 · 2019: 6 · 2018: 11 · 2017: 12 · 2016: 13 · 2015: 20 · 2014: 16 · 2013: 14 · 2012: 19
- FWCI
- 1.98
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Hypertension (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of General Medical Sciences (GM061731, R01GM061731)
- Topics
- Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Health and Disease Prevention
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Eicosanoids and Hypertension Pharmacology
- Keywords
- nitric oxide, cardiovascular disease, nitric oxide signaling, nitroglycerin, reactive nitrogen species, smooth muscle relaxation, platelet aggregation, vascular smooth muscle cell proliferation, inflammation
- MeSH terms
- Cardiovascular Agents, Cardiovascular Diseases, Cardiovascular System, Endothelium, Humans, Hypertension, Nitric Oxide, Signal Transduction, Reactive Oxygen Species, Reactive Nitrogen Species, Atherosclerosis
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