Nitric oxide and its role in the cardiovascular system

Loscalzo, Joseph; Welch, George N.

doi:10.1016/s0033-0620(05)80001-5

Cited by 532 publications

(315 citation statements)

References 135 publications

Supporting

Mentioning

286

Contrasting

Unclassified

Order By: Relevance

“…The principle vasodilating agent generated in conduit vessels is currently thought of as being NO (41). We proposed that an increased production of basal NO would lower the contractions to all of the agonists used in this study.…”

Section: Discussionmentioning

confidence: 95%

Developmental programming of lipid metabolism and aortic vascular function in C57BL/6 mice: a novel study suggesting an involvement of LDL-receptor

Chechi

McGuire²,

Cheema³

2009

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

Chechi K, McGuire JJ, Cheema SK. Developmental programming of lipid metabolism and aortic vascular function in C57BL/6 mice: a novel study suggesting an involvement of LDL-receptor. Am J Physiol Regul Integr Comp Physiol 296: R1029 -R1040, 2009. First published February 4, 2009 doi:10.1152/ajpregu.90932.2008We have previously shown that a maternal high-fat diet, rich in saturated fatty acids (SFA), alters the lipid metabolism of their adult offspring. The present study was designed to investigate 1) whether alterations in hepatic LDL-receptor (LDL-r) expression may serve as a potential mechanism of developmental programming behind the altered lipid metabolism of the offspring, 2) whether altered lipid metabolism leads to aortic vascular dysfunction in the offspring, 3) whether deleterious effects of SFA exposure preweaning are influenced by postweaning diet, and 4) whether gender-specific programming effects are observed. Female C57Bl/6 mice were fed a high-SFA diet or regular chow during gestation and lactation while their pups, both male and female, received either SFA or a chow diet after weaning. Male offspring obtained from mothers fed an SFA diet and those who continued on chow postweaning had higher plasma triglycerides and total cholesterol, whereas female offspring had higher plasma total and LDL cholesterol levels, lower hepatic LDL-r mRNA expression, and reduced aortic contractile responses compared with the offspring that were fed chow throughout the study. A comparison of the postweaning diet revealed significantly lower hepatic LDL-r expression along with significantly higher plasma LDL-cholesterol concentration in the female offspring that were obtained from mothers fed an SFA diet and who continued on an SFA diet postweaning, compared with the female offspring that were obtained from mothers fed an SFA diet but who continued on chow postweaning. In conclusion, we report a novel observation of hepatic LDL-r-mediated programming of altered lipid metabolism, along with aortic vascular dysfunction, in the female offspring of mothers fed a high-SFA diet. Male offspring only exhibited dyslipidemia, suggesting gender-mediated programming. This study further highlighted the role of postweaning diets in overriding the effects of maternal programming. fetal programming; plasma lipids; hepatic LDL-receptor; dietary fats; cardiovascular disease RECENT EVIDENCE BASED ON THE developmental origins of health and disease hypothesis suggests that early nutrition can be critical in determining the cardiovascular health of an individual (43, 44). According to this hypothesis, which was originally known as Barker's hypothesis, an adverse maternal nutrition during gestation can create a stressed environment for the developing fetus. The fetus responds to this nutritional stress by programming its own growth in a way that could increase its risk of developing metabolic disorders in later life (6 -8). Considering that a typical Western diet is rich in dietary fat content (17), especially saturated fatty acids (SFA), s...

show abstract

Section: Discussionmentioning

confidence: 95%

Developmental programming of lipid metabolism and aortic vascular function in C57BL/6 mice: a novel study suggesting an involvement of LDL-receptor

Chechi

McGuire²,

Cheema³

2009

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

show abstract

“…The eNOS, encoded by the NOS3 gene, is the principal source of NO within cardiovascular cells. Vascular NO derived from eNOS modulates numerous essential vascular functions, including regulation of blood pressure, inhibition of platelet aggregation, and inhibition of leukocyte adhesion, among others (see review 20 ). While we focus on eNOS regulation by S1P receptor systems in this article, readers are invited to another review paper in which we discussed more general aspects of the eNOS/NO system.…”

Section: Cellular Sources Of Blood Sphingosine-1-phosphate That Modulmentioning

confidence: 99%

“…Since platelet-related molecules other than S1P, including thrombin, 20 are also able to activate eNOS, it remains to be determined whether or not S1P activates eNOS in the face of vascular coagulation in vivo. Yet in blood vessels in which S1P exerts overall vasoconstriction responses, the local production of S1P by platelets might help reduce bleeding by decreasing local blood flow.…”

Section: Pathophysiological Implications Of Sphingosine-1-phosphate-imentioning

confidence: 99%

Sphingosine-1-phosphate and modulation of vascular tone

Igarashi¹,

Michel²

2009

Cardiovascular Research

100

View full text Add to dashboard Cite

Sphingosine-1-phosphate (S1P) is a phosphorylated product of sphingosine, the core structure of the class of lipids termed sphingolipids. S1P is a naturally occurring lipid metabolite, and usually is present at a concentration of a few 100 nanomolar in human sera. S1P has been found to exert a diverse set of physiological and pathophysiological responses in mammalian tissues through the activation of heterotrimeric G-proteins that in turn modulate the activity of various downstream effecter molecules. In blood vessels, vascular endothelial cells and smooth muscle cells express specific receptors for S1P that modulate vascular tone. This article will provide a brief overview of S1P metabolism in the vasculature and will discuss some of the pathways whereby S1P regulates intracellular signal transduction pathways in endothelial and smooth muscle cells, leading to the activation of both vasorelaxation and vasoconstriction responses.

show abstract

“…Nitric oxide (NO), essential for the proper functioning of the cardiovascular system, is derived from L-arginine by NO synthase (NOS) in endothelial cells. NO synthase inhibition produces various cardiovascular abnormalities and ventricular contractile dysfunction (Loscalzo and Welch, 1995;Dickinson and Forman, 2002). Although no previous report has investigated TAS, TOS, and OSI as biomarkers of oxidative stress and antioxidant defence related to treating the rabbits with enrofloxacin, a possible explanation for this might be that free oxidant radicals are not produced.…”

Section: Discussionmentioning

confidence: 99%

Cardiotoxic effects of enrofloxacin on electrophysiological activity, cardiac markers, oxidative stress, and haematological findings in rabbits

Durgut¹,

Öztürk²,

Nacar³

et al. 2016

Turk J Zool

View full text Add to dashboard Cite

IntroductionProlongation of the QT interval is commonly used as a surrogate marker of torsades de pointes (TdP), which is a known clinical risk factor for the development of severe, life-threatening, ventricular arrhythmias (Abi-Gerges et al., 2004). Noncardiovascular drug-induced prolongation of the QT interval is often associated with the onset of TdP (Haverkamp et al., 2000;De Ponti et al., 2001). Fluoroquinolones are among the drugs of choice for the treatment of common bacterial infections due to their wide spectrum against respiratory, gastrointestinal, and genitourinary pathogens (Elmas et al., 2006). QT interval prolongation is also a class effect of fluoroquinolones but there are great differences between the various members of this group (Camm, 2005). Thus, there are significant differences in the potency to prolong QT interval among the fluoroquinolones and the risk of arrhythmia varies between drugs and with co-risk factors (Frothingham, 2001;Owens and Ambrose, 2002). Because a QT prolongation and potentially fatal ventricular arrhythmias associated with quinolones such as grepafloxacin due to several cases of sudden death and TdP have been encountered retrospectively, enrofloxacin needs to be further investigated in detail. Therefore, the purpose of this study was to investigate the effect of normal and high doses of enrofloxacin on basal electrocardiographic parameters including heart rate (HR), P, QRS, QT, and RR intervals and corrected QT (QTc) values as well as biochemical and haematological findings in healthy conscious rabbits. Materials and methods ApprovalsThis study was approved by the Institutional Laboratory Animal Care and Use Committee of Mustafa Kemal University (2011 -01 -09). ChemicalsAll chemicals were obtained from Sigma Chemical Co, and solutions were prepared fresh daily from concentrated stock solutions. Animal preparationAfter 1 week of quarantine and acclimatisation, a total of 21 healthy New Zealand rabbits of both sexes, 12-18 months old, and of 2-4 kg body weight were used. The rabbits were housed individually in stainless-steel wire mesh cages and provided with food and water ad libitum. All rabbits were

show abstract

Nitric oxide and its role in the cardiovascular system

Cited by 532 publications

References 135 publications

Developmental programming of lipid metabolism and aortic vascular function in C57BL/6 mice: a novel study suggesting an involvement of LDL-receptor

Developmental programming of lipid metabolism and aortic vascular function in C57BL/6 mice: a novel study suggesting an involvement of LDL-receptor

Sphingosine-1-phosphate and modulation of vascular tone

Cardiotoxic effects of enrofloxacin on electrophysiological activity, cardiac markers, oxidative stress, and haematological findings in rabbits

Contact Info

Product

Resources

About