Nitric Oxide in the Vasculature: Where Does It Come From and Where Does It Go? A Quantitative Perspective

Chen, Kejing; Pittman, Roland N.; Popel, Aleksander S.

doi:10.1089/ars.2007.1959

Cited by 251 publications

(191 citation statements)

References 114 publications

(124 reference statements)

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“…For example, cytochrome P450 reductase is an eNOS-independent endothelial generator of NO, at least in arteries of the spontaneously hypertensive rat, which may be a compensatory mechanism to restore NO bioavailability when release from its canonical source (eNOS) is deficient. 29,[53][54][55] S-nitrosothiols can also act as a source of NO. Endothelial cells can form such S-nitrosothiols from either exogenous donors (eg, S-nitrosoglutathione) or NO produced by eNOS; they are considered to be intermediates in the storage and transport of NO.…”

Section: Post-translational Modulation Of Enos Activitymentioning

confidence: 99%

“…S-nitrosothiols are stable under physiological conditions; however, they liberate NO when exposed to trace amounts of redox-sensitive transition metal ions (eg, Cu + or Fe 2+ ) in the presence of thiol-reducing agents (eg, reduced glutathione, l-cysteine and hydrogen sulfide), the levels of which are reduced by oxidative stress. 29,53,54,[56][57][58] …”

Section: Post-translational Modulation Of Enos Activitymentioning

confidence: 99%

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Thirty Years of Saying NO

Vanhoutte

Zhao

et al. 2016

Circulation Research

328

156

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T he historical demonstration by Furchgott and Zawadzki 1 that removal of the endothelium abrogates the in vitro vasodilator effect of acetylcholine has led to the identification 30 years ago of nitric oxide (NO) as a major endogenous local regulator of vascular tone. [2][3][4][5][6][7][8][9][10] When the ability of endothelial cells to produce NO is blunted, the ensuing vascular dysfunction sets the stage for the occurrence of cardiovascular disease in general, and atherosclerosis in particular. [11][12][13][14][15] This review focuses, stepby-step, on the bioavailability (production, action, and disposition) of endothelium-derived NO as local regulator of vascular tone in health and disease. Obviously, there is much more than NO in the control of the degree of contraction of underlying vascular smooth muscle cells exerted by the endothelial cells. Indeed, they generate also prostacyclin and hyperpolarizing signals (initiating endothelium-dependent hyperpolarization [EDH] and thus relaxation) and produce vasoconstrictor mediators (endothelium-derived contracting factors and the peptide endothelin-1); those have been discussed elsewhere in detail. 15-22 Endothelial Sources of NO NO SynthaseThree NO synthase (NOS) isozymes, which are encoded by different genes, catalyze the production of NO from l-arginine: neuronal NOS (or NOS-1), cytokine-inducible NOS (iNOS or NOS-2), and endothelial NOS (eNOS or NOS-3).6,23-25 Although iNOS can be induced (by lipopolysaccharides and inflammatory cytokines) and neuronal NOS can be present in the blood vessel

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Section: Post-translational Modulation Of Enos Activitymentioning

confidence: 99%

Section: Post-translational Modulation Of Enos Activitymentioning

confidence: 99%

Thirty Years of Saying NO

Vanhoutte

Zhao

et al. 2016

Circulation Research

328

156

View full text Add to dashboard Cite

show abstract

“…NO has a short half-life as it is scavenged by superoxide anions (Rubanyi and Vanhoutte, 1986) or quickly oxidized by O 2 , reactive oxygen species (ROS), and hemoglobin to form nitrate or nitrite (Chen et al, 2008). A major mechanism of NO formation is by nitric oxide synthase (NOS) [including neuronal (nNOS; NOS I), inducible (iNOS; NOS II) and endothelial (eNOS; NOS III) isoforms], which involves a series of redox reactions, with L-arginine being the substrate and L-citrulline and NO the end-products (Palmer et al, 1988;Alderton et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

Endothelial Nitric Oxide Synthase-Independent Release of Nitric Oxide in the Aorta of the Spontaneously Hypertensive Rat

Zhao

Vanhoutte

Leung

2012

J Pharmacol Exp Ther

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In the aorta of male spontaneously hypertensive rats (SHR), but not in that of normotensive Wistar-Kyoto rats (WKY), contractions to phenylephrine obtained in the presence of L-NAME [inhibitor of nitric oxide synthase (NOS)] and indomethacin (inhibitor of cyclooxygenase) are inhibited by an unknown endothelium-derived factor. The present study aimed to identify the mechanism underlying this endothelium-dependent inhibition in the SHR aorta. Aortic rings of male SHR and WKY, with and without endothelium, were suspended in organ chambers in the presence of indomethacin and L-NAME for the measurement of isometric tension. Contractions to phenylephrine were smaller in SHR aortae with endothelium than in those without, but were similar in the two types of preparations of WKY aortae.The endothelium-dependent, NOS-independent inhibition of phenylephrine-induced contraction was abolished by oxyhemoglobin [extracellular NO scavenger], carboxy-PTIO (NO scavenger) and ODQ (inhibitor of soluble guanylyl cyclase). It was unmasked not only by indomethacin but also by apocynin (antioxidant), but inhibited by diphenyleneiodonium (inhibitor of flavoproteins including cytochrome P450 reductase). The cytochrome P450 reductase protein expression was similar in SHR and WKY aortae. However, the level of nitrate and nitrite, substrates of cytochrome P450 reductase, were higher in SHR than WKY plasma and aortae. Therefore, in SHR but not WKY aortae, eNOS-independent NO is formed by cytochrome P450 reductase.

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“…Although the increase and decrease of NO production may have various influences [21], NO regulates many important processes (e.g. vascular tone, blood flow, insulin sensitivity and resistance) in the entire body and plays a key role in many pathologies like hypertension, atherosclerosis and angiogenesis-associated disorders [21,22]. NO also regulates many neurological processes influencing behavior and cognitive function.…”

Section: Resultsmentioning

confidence: 99%

Low molecular fucoidan and its macromolecular complex with bee venom melittin

Mavlonov¹,

Lee²,

Lee³

et al. 2011

ABB

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Low molecular weight (LMW) fucoidan, obtained by free radical depolymerization of high molecular polysaccharide extract of brown algae Hizikia fusiformis, was complexed with HPLC purified bee venom melittin. Water soluble form of the LMW fucoidan:melittin complex shows increased anti-inflammatory activity, inhibiting the production of nitric oxide in murine macrophage cell line Raw 264.7. The LMW fucoidan: melitin complex obtained in this study showed good biological activities, resulting in 2-fold reduction of the melittin toxicity. The fucoidan:melittin macromolecular complex obtained should be useful in future therapeutic applications.

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Nitric Oxide in the Vasculature: Where Does It Come From and Where Does It Go? A Quantitative Perspective

Cited by 251 publications

References 114 publications

Thirty Years of Saying NO

Thirty Years of Saying NO

Endothelial Nitric Oxide Synthase-Independent Release of Nitric Oxide in the Aorta of the Spontaneously Hypertensive Rat

Low molecular fucoidan and its macromolecular complex with bee venom melittin

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