Tetrahydrobiopterin: coupling nitric oxide and redox signalling in cardiovascular disease

2012 ◽  
Vol 56 (5-6) ◽  
pp. 322
Author(s):  
Keith M. Channon
Keyword(s):  
Nitric Oxide ◽  
Cardiovascular Disease ◽  
Redox Signalling

NITRIC OXIDE, FREE RADICALS AND CELL SIGNALLING IN CARDIOVASCULAR DISEASE

1997 ◽  
Vol 25 (3) ◽  
pp. 384S-384S
Author(s):  
Victor M. Darley-Usmar ◽  
Joanne McAndrew ◽  
Roger White ◽  
Rakesh Patel ◽  
Doug Moellering ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cardiovascular Disease ◽  
Free Radicals ◽  
Cell Signalling

827: African-Americans, preeclampsia and future cardiovascular disease: Is nitric oxide the missing link?

2008 ◽  
Vol 199 (6) ◽  
pp. S233
Author(s):  
Kedra Wallace ◽  
Adrienne Wells ◽  
William Bennett
Keyword(s):  
Nitric Oxide ◽  
Cardiovascular Disease ◽  
African Americans ◽  
Missing Link

scholarly journals BETAINE INDUCED RELEASE OF TISSUE FACTOR PATHWAY INHIBITOR AND NITRIC OXIDE: IMPLICATIONS IN THE MANAGEMENT OF CARDIOVASCULAR DISEASE

2006 ◽  
Vol 20 (4) ◽  
Author(s):  
Omer Iqbal ◽  
D Fareed ◽  
J Cunanan ◽  
D Hoppensteadt ◽  
J Messadek ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cardiovascular Disease ◽  
Tissue Factor ◽  
Tissue Factor Pathway Inhibitor ◽  
Tissue Factor Pathway

scholarly journals Nitric Oxide and Cardiovascular Disease

1995 ◽  
Vol 2 (3) ◽  
pp. 73-79
Author(s):  
Motoyuki Nakamura ◽  
Katsuhiko Hiramori
Keyword(s):  
Nitric Oxide ◽  
Cardiovascular Disease

Endothelial nitric oxide and cardiovascular disease

1994 ◽  
Vol 235 (4) ◽  
pp. 317-327 ◽  
Author(s):  
Å. Wennmalm
Keyword(s):  
Nitric Oxide ◽  
Cardiovascular Disease ◽  
Endothelial Nitric Oxide

scholarly journals Mechanisms of lead-induced hypertension and cardiovascular disease

2008 ◽  
Vol 295 (2) ◽  
pp. H454-H465 ◽  
Author(s):  
Nosratola D. Vaziri
Keyword(s):  
Nitric Oxide ◽  
Cardiovascular Disease ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Plasminogen Activator ◽  
Lead Exposure ◽  
Molecular Mechanisms ◽  
Subsequent Development ◽  
Endothelial Injury ◽  
Nitric Oxide Signaling

Lead is a ubiquitous environmental toxin that is capable of causing numerous acute and chronic illnesses. Population studies have demonstrated a link between lead exposure and subsequent development of hypertension (HTN) and cardiovascular disease. In vivo and in vitro studies have shown that chronic lead exposure causes HTN and cardiovascular disease by promoting oxidative stress, limiting nitric oxide availability, impairing nitric oxide signaling, augmenting adrenergic activity, increasing endothelin production, altering the renin-angiotensin system, raising vasoconstrictor prostaglandins, lowering vasodilator prostaglandins, promoting inflammation, disturbing vascular smooth muscle Ca2+ signaling, diminishing endothelium-dependent vasorelaxation, and modifying the vascular response to vasoactive agonists. Moreover, lead has been shown to cause endothelial injury, impede endothelial repair, inhibit angiogenesis, reduce endothelial cell growth, suppress proteoglycan production, stimulate vascular smooth muscle cell proliferation and phenotypic transformation, reduce tissue plasminogen activator, and raise plasminogen activator inhibitor-1 production. Via these and other actions, lead exposure causes HTN and promotes arteriosclerosis, atherosclerosis, thrombosis, and cardiovascular disease. In conclusion, studies performed in experimental animals, isolated tissues, and cultured cells have provided compelling evidence that chronic exposure to low levels of lead can cause HTN, endothelial injury/dysfunction, arteriosclerosis, and cardiovascular disease. More importantly, these studies have elucidated the cellular and molecular mechanisms of lead's action on cardiovascular/renal systems, a task that is impossible to accomplish using clinical and epidemiological investigations alone.

Hyperinsulinemia and impaired leptin-adiponectin ratio associate with endothelial nitric oxide synthase polymorphisms in subjects with in-stent restenosis

2008 ◽  
Vol 294 (5) ◽  
pp. E978-E986 ◽  
Author(s):  
Elena Galluccio ◽  
PierMarco Piatti ◽  
Lorena Citterio ◽  
Pietro C. G. Lucotti ◽  
Emanuela Setola ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cardiovascular Disease ◽  
Endothelial Dysfunction ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Stent Restenosis ◽  
Nos3 Gene ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide ◽  
In Stent Restenosis

Little is known about the association of endothelial nitric oxide synthase (NOS3) gene polymorphisms and the presence of insulin resistance and the early evolution of atherosclerosis in nondiabetic subjects with cardiovascular disease (CAD) and stent implantation. The present study was performed in an attempt to better understand whether metabolic, endothelial, and angiographic findings characteristic of subjects with cardiovascular disease and in-stent restenosis are related to NOS3 variants. This is a case-control study performed from 2002 to 2006. All subjects admitted to the study were recruited in the Nord-Centre of Italy, most from Milan and its surrounding towns. Measures of glucose tolerance, insulin sensitivity, markers of endothelial dysfunction, forearm vasodilation, and adipokine levels were determined and associated to the frequency of two single-nucleotide polymorphisms of NOS3, i.e., Glu298Asp (rs1799983, G/T) and rs753482 (intron 18 A/C). A total of 747 subjects, not known to have diabetes, were evaluated: 333 subjects had asymptomatic CAD, 106 subjects had unstable angina and were evaluated for in-stent restenosis 6 mo after stent placement, and 308 were control subjects. The presence of TT and CC minor alleles was significantly greater in case groups compared with control subjects. At phenotypic level, subjects with the polymorphisms were characterized by hyperinsulinemia and reduced reactive hyperemia, whereas increased leptin and decreased adiponectin levels were present in subjects with restenosis in the presence of reduced minimal lumen diameter and length of stenosis almost doubled. Hyperinsulinemia, endothelial dysfunction, and a more atherogenic profile seem to be peculiar features of subjects with asymptomatic CAD and restenosis carrying NOS3 gene variants.

Therapeutic role of nitric oxide donors in the treatment of cardiovascular disease

1994 ◽  
Vol 19 (7) ◽  
pp. 665 ◽  
Author(s):  
A.M. Lefer ◽  
D.J. Lefer
Keyword(s):  
Nitric Oxide ◽  
Cardiovascular Disease ◽  
Nitric Oxide Donors ◽  
Therapeutic Role
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