Vascular endothelial cells synthesize nitric oxide from L-arginine

Palmer, Richard; Ashton, David; Moncada, Salvador

doi:10.1038/333664a0

Cited by 4,405 publications

(1,964 citation statements)

References 12 publications

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“…Examples include NO, prostacyclin (PGI 2 ) and endothelium derived hyperpolarising factor (EDHF) 4 . NO is the best characterised relaxing factor and is derived from transformation of L-arginine into citrulline via NO synthase (NOS) which is constitutively expressed in endothelial cells [10][11][12][13] . NO may also be produced and released under the influence of stimuli such as acetylcholine, bradykinin, substance P, serotonin, and mechanical shear stresses 4 .…”

Section: Endothelial Dysfunctionmentioning

confidence: 99%

Drug Treatment of Hypertension: Focus on Vascular Health

Cameron

Lang

Touyz

2016

Drugs

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Hypertension, the most common preventable risk factor for cardiovascular disease and death, is a growing health burden. Serious cardiovascular complications result from target organ damage including cerebrovascular disease, heart failure, ischaemic heart disease and renal failure. While many systems contribute to blood pressure elevation, the vascular system is particularly important, because vascular dysfunction is a cause and consequence of hypertension. Hypertension is characterised by a vascular phenotype of endothelial dysfunction, arterial remodelling, vascular inflammation and increased stiffness. Antihypertensive drugs that influence vascular changes associated with high blood pressure have greater efficacy for reducing cardiovascular risk than drugs that reduce blood pressure but have little or no effect on the adverse vascular phenotype. Angiotensin converting enzyme Key Points• Hypertension is characterized by a vascular phenotype of endothelial dysfunction and structural remodeling.• Anti-hypertensive drugs that target the vascular changes associated with hypertension appear to be most efficacious• New anti-hypertensive drugs should promote vascular health as well as reducing blood pressure 3

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Section: Endothelial Dysfunctionmentioning

confidence: 99%

Drug Treatment of Hypertension: Focus on Vascular Health

Cameron

Lang

Touyz

2016

Drugs

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“…The endothelium exerts a multimodal regulation of vascular smooth muscle tone and structure by the release of nitric oxide (NO), endothelium-derived hyperpolarizing factor, and prostacyclin. NO is generated from L -arginine catalyzed by NO synthases (Palmer et al, 1988;Moncada and Higgs, 1993). One of these isoenzymes, endothelial NO synthase (eNOS), is constitutively expressed in endothelial cells .…”

Section: Introductionmentioning

confidence: 99%

Superoxide as a Messenger of Endothelial Function

Ullrich

Bachschmid²

2000

Biochemical and Biophysical Research Communications

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“…iNOS contributes to the formation of nitric oxide (NO) from L-arginine (8). Locally produced NO relaxes vascular smooth muscle and expression of iNOS and excessive production of nitric oxide in the blood vessel wall mediates vasodilation resulting in hypotension during septic shock (3,9).…”

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confidence: 99%

Bactericidal/permeability‐increasing protein inhibits endotoxin‐induced vascular nitric oxide synthesis

Ciornei

Egesten

Engström

et al. 2002

Acta Anaesthesiol Scand

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Background: Endotoxin (lipopolysaccharide, LPS) up‐regulates inducible nitric oxide synthase (iNOS) in blood vessels during septic shock. This promotes the production of nitric oxide (NO), leading to dilation of the vessels. The aim of the study was to investigate the effects of the LPS‐binding endogenous antibiotic bactericidal/permeability‐increasing protein (BPI) on the action of LPS on the blood vessels wall and to identify possible influence on underlying NO‐related mechanisms.Methods: Isolated segments of rat thoracic aorta and cultured primary smooth muscle cells were incubated for 5–48 h in the presence of the following combinations of compounds: (a) LPS; (b) interleukin‐1β (IL‐1β); (c) BPI; (d) BPI + LPS; (e) BPI + IL‐1β or (f) neither BPI, LPS nor IL‐1β (control). After incubation of intact segments, we measured smooth muscle contraction in response to phenylephrine and accumulation of the NO end products nitrate and nitrite in surrounding medium. Western blot was used to assess the levels of inducible nitric oxide synthase (iNOS) in cultured cells.Results: Both LPS and IL‐1β decreased contractility and increased NO production, as well as iNOS. Co‐incubation with BPI attenuated all the effects of LPS but only the effects of prolonged exposure to IL‐1β in cultured cells.Conclusion: We conclude that BPI attenuates the LPS‐induced changes in vascular reactivity by inhibiting the expression of iNOS resulting in decreased NO formation and restored responsiveness to vasoconstrictors. The data suggest that BPI can prevent circulatory disturbances during Gram‐negative sepsis.

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Vascular endothelial cells synthesize nitric oxide from L-arginine

Cited by 4,405 publications

References 12 publications

Drug Treatment of Hypertension: Focus on Vascular Health

Drug Treatment of Hypertension: Focus on Vascular Health

Superoxide as a Messenger of Endothelial Function

Bactericidal/permeability‐increasing protein inhibits endotoxin‐induced vascular nitric oxide synthesis

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