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The DOI matches its Crossref record; 41 of the 41 references it cites were found in a registry or an index.

Vascular nitric oxide: Beyond eNOS

Open access
Zhao, Yingzi, Vanhoutte, Paul M., Leung, Susan W.S.·2015·Journal of Pharmacological Sciences

Abstract

As the first discovered gaseous signaling molecule, nitric oxide (NO) affects a number of cellular processes, including those involving vascular cells. This brief review summarizes the contribution of NO to the regulation of vascular tone and its sources in the blood vessel wall. NO regulates the degree of contraction of vascular smooth muscle cells mainly by stimulating soluble guanylyl cyclase (sGC) to produce cyclic guanosine monophosphate (cGMP), although cGMP-independent signaling [S-nitrosylation of target proteins, activation of sarco/endoplasmic reticulum calcium ATPase (SERCA) or production of cyclic inosine monophosphate (cIMP)] also can be involved. In the blood vessel wall, NO is produced mainly from l-arginine by the enzyme endothelial nitric oxide synthase (eNOS) but it can also be released non-enzymatically from S-nitrosothiols or from nitrate/nitrite. Dysfunction in the production and/or the bioavailability of NO characterizes endothelial dysfunction, which is associated with cardiovascular diseases such as hypertension and atherosclerosis.

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Metadata

Authors
Zhao, Y., Vanhoutte, P. M., & Leung, S. W. S.
Venue
Journal of Pharmacological Sciences
Publisher
Elsevier BV
Published
2015-10
Volume
129
Issue
2
Pages
83-94
ISSN
1347-8613 (ISSN-L)
OpenAlex
W2181241483
Cited by
826
References
41
FWCI
37.02
Type
journal article
Language
en
Open access
gold

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CoChat. (2026). Citation check: Vascular nitric oxide: Beyond eNOS. https://app.cochat.ai/papers/10.1016/j.jphs.2015.09.002
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Zhao, Y., Vanhoutte, P. M., & Leung, S. W. S. (2015). Vascular nitric oxide: Beyond eNOS. Journal of Pharmacological Sciences. https://doi.org/10.1016/j.jphs.2015.09.002

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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