Regulation of nitric oxide production from macrophages by lipopolysaccharide and catecholamines

David, S.; Qui, Min; Krishnaswamy, Guha; Li, Chuanfu; Stone, William L.

doi:10.1016/s1089-8603(02)00148-9

Cited by 103 publications

(74 citation statements)

References 27 publications

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“…For example, there is evidence that ␤-adrenoceptors can influence LPS-induced production of a variety of proand anti-inflammatory cytokines (for review see Ref. 21) and inducible nitric oxide (NO) synthase-mediated NO production (4,5). It is notable that treatment with propranolol 24 h after the onset of LPS infusion reduced, but did not abolish, the tachycardia and hindquarter vasodilatation.…”

Section: Discussionmentioning

confidence: 99%

Involvement of CB₁-receptors and β-adrenoceptors in the regional hemodynamic responses to lipopolysaccharide infusion in conscious rats

Gardiner¹,

March²,

Kemp³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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A possible involvement of endocannabinoids in a chronic model of endotoxemia was assessed by measuring the regional (renal, mesenteric, hindquarters) hemodynamic responses to continuous 24-h LPS infusion (150 g ⅐ kg Ϫ1 ⅐ h Ϫ1 ) in conscious, male Sprague-Dawley rats, in the absence or presence of the cannabinoid (CB 1) receptor antagonist AM-251 (3 mg/kg). AM-251 inhibited the tachycardic and hindquarters vasodilator effects of LPS, but did not influence the other hemodynamic changes. In subsequent experiments, it was shown that the tachycardic and hindquarters vasodilator effects of LPS were also inhibited by the nonselective ␤-adrenoceptor antagonist propranolol. In addition, the late (at 24 h) hindquarters vasodilator effects of LPS were inhibited by the ␤2-adrenoceptor antagonist ICI-118551. Against the background of our previous work showing ␤-adrenoceptor involvement in the cardiovascular effects of exogenous cannabinoids, we conclude that AM-251 may have been inhibiting endocannabinoid-modulated, sympathoadrenal-mediated activation of vasodilator ␤-adrenoceptors in LPS-infused rats rather than suppressing a direct vasodilator action of endocannabinoids.AM-251; endotoxemia; vasodilatation THE SYSTEMIC RESPONSE TO BACTERIAL infection, often referred to as sepsis, involves complex pathogenetic mechanisms and associated cardiovascular changes (26). Before the development of septic shock, there may be a hyperdynamic phase of sepsis with high cardiac output and peripheral vasodilatation (26). The underlying causes of the vasodilatation are multifactorial, involving the loss of vascular sensitivity to vasoconstrictors (25), some of which may be released through nonbaroreflex-mediated processes (39) and possibly contributed to by disorders of baroreflex control (29). In addition, there are numerous potential vasodilator mediators reported to be involved in the cardiovascular sequelae of sepsis (25).Endotoxemia induced by the administration of the bacterial cell wall product, LPS, to experimental animals is often used to model some of the pathophysiological changes occurring in sepsis. In a model of endotoxemia, involving a large bolus dose of LPS in anesthetized male Sprague-Dawley rats, Varga et al. -141716A) prevented the fall in mean arterial blood pressure. In addition, LPS stimulated the production of endocannabinoids by platelets and macrophages, although increased circulating levels of these substances were not directly demonstrated in LPS-treated rats (33). The same group has also shown an involvement of endogenous cannabinoids in the hypotension associated with hemorrhagic shock (35) and after myocardial infarction (34). In vitro studies (28) have shown cannabinoids cause vasodilatation by a variety of mechanisms, including release of endothelium-derived hyperpolarizing factor, activation of potassium channels, inhibition of calcium channels, direct effects of cannabinoid receptors on vascular smooth muscle, release of mediators from sensory nerves, and presynaptic inhibition of norepinephrine release. ...

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Section: Discussionmentioning

confidence: 99%

Involvement of CB₁-receptors and β-adrenoceptors in the regional hemodynamic responses to lipopolysaccharide infusion in conscious rats

Gardiner¹,

March²,

Kemp³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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“…CRP may also increase NO production by acting as a proinflammatory stimulus to phagocytic cells by binding to the Fc␥RII receptor (Bharadwaj et al, 1999) or stimulating monocyte release of inflammatory cytokines such as IL-1␤, IL-6, and tumor necrosis factor-␣ (Ballou and Lozanski, 1992). ␤-AR stimulation may also enhance iNOS expression and NO production through other mechanisms, including enhancing the IL-1␤ effect by stabilizing the iNOS message (Gustafsson and Brunton, 2000), increasing macrophage arginase activity (Bernard et al, 2000), enhancing L-arginine transport in activated macrophages (Lin et al, 2005), and producing a synergic effect with lipopolysaccharide or cytokines (Kurosaki et al, 2000;Chi et al, 2003). Further studies are needed to illustrate potential interactions between proinflammatory mediators (CRP, cytokines) and iNOS in reinforcing the inflammatory response triggered by chronic ␤-AR stimulation.…”

Section: How Does ␤-Ar Stimulation Induce Inos Overexpression?mentioning

confidence: 99%

Chronic β-Adrenergic Receptor Stimulation Induces Cardiac Apoptosis and Aggravates Myocardial Ischemia/Reperfusion Injury by Provoking Inducible Nitric-Oxide Synthase-Mediated Nitrative Stress

Jiao²,

Gao³

et al. 2006

J Pharmacol Exp Ther

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The present study provides evidence that inducible nitric-oxide synthase (iNOS)-mediated nitrative stress plays a pivotal role in chronic ␤-adrenergic receptor (AR) stimulation-induced cardiac damage. In mice, 14 days of isoproterenol (ISO) stimulation via an osmotic minipump induced an up-regulation of iNOS as evidenced by increases in mRNA, protein expression, and immunochemical staining of myocardial iNOS. Serum level of C-reactive protein, an inflammatory mediator, was also markedly increased. Under chronic ISO stimulation, the up-regulated iNOS produced a significantly increased amount of nitric oxide (NO) and its byproduct, peroxynitrite, in the circulation and heart and subsequently resulted in an accelerated myocardial apoptosis. Forty-minute myocardial ischemia (MI) and 24-h reperfusion (R) further increased NO production and peroxynitrite formation and resulted in an enlarged infarct size in mice receiving chronic ISO stimulation. However, the treatment with a selective iNOS inhibitor [N-(3-(aminomethyl) benzyl)acetamidine] (1400W) or the use of a genetic modified animal (iNOSknockout mice) markedly reduced iNOS-mediated production of NO and formation of peroxynitrite and consequently significantly decreased myocardial apoptosis and infarct size, showing a crucial link between iNOS-mediated nitrative stress and myocardial injury. In conclusion, chronic ␤-AR stimulation upregulates iNOS expression and increases NO production in the heart, which subsequently markedly enhances formation of reactive nitrogen species/peroxynitrite in the heart, thereby eliciting myocardial apoptosis and potentiating MI/R injury.

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“…It suggests not only that the presence of IFN-c is highly required so that 6-CMMP reduces NO production but also that the pathway by which this compound acts on NO levels is different from cellular proliferation pathway when BCG stimulus is applied. The characteristics demonstrated by 6-CMMP are appropriate for decreasing NO overproduction in inflammation processes, which may avoid the tissue damage and the carcinogenic action of free radicals (24,31). It may be pointed out therefore that 6-CMMP might act as an antiinflammatory agent.…”

Section: Discussionmentioning

confidence: 99%

“…The production of NO was estimated from the accumulation of NO 3 ) and NO 2 ) in J774A.1 supernatants using the Griess reagent, as previously described (18,31). Briefly, equal volumes (100 lL) of nitrite samples for standard curve and Griess reagent (1% sulphanilamide plus 0.1% a-naphtylamine (v ⁄ v) in 2.5% phosphoric acid) (Sigma Chemical Laboratories, St Louis, MO, USA) were mixed and incubated at room temperature for 10 min.…”

Section: Determination Of No Productionmentioning

confidence: 99%

Modulatory Effects of 6‐Carboxymethylthiopurine on Activated Murine Macrophages

et al. 2008

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The immunological activity of macrophages against pathogens in hosts includes the phagocytosis and the production of nitric oxide. We report herein the investigation of the effect of 6‐carboxymethylthiopurine on nitric oxide production by murine macrophages as well as its effect on the cell viability and proliferation after stimulus with Mycobacterium bovis bacille Calmette–Guérin, interferon‐gamma or a combination of both. J774A.1 macrophages stimulated or not by bacille Calmette–Guérin (20 μg/mL), interferon‐gamma or both, were cultured in the presence of 6‐carboxymethylthiopurine (125, 250 and 500 μm). Nitric oxide production was measured by the Griess method and cell viability/proliferation by the diphenyltetrazolium assay [3‐(4, 5‐dimethylthiazol‐2‐yl)‐2, 5‐diphenyltetrazolium bromide]. We observed an increase of J774A.1 cell proliferation after stimulus with bacille Calmette–Guérin at 125, 250 and 500 μm (69.1, 124.0 and 89.7%, respectively) and with interferon‐gamma at 125 and 250 μm (64.8% and 61.7%, respectively) (p < 0.05). In all cultures treated with 6‐carboxymethylthiopurine, interferon‐gamma‐activated nitric oxide production by J774A.1 cells decreased as well as when subjected to interferon‐gamma plus bacille Calmette–Guérin stimuli at 500 μm (p < 0.05). Altogether these data point to an anti‐inflammatory effect of 6‐carboxymethylthiopurine on stimulated macrophages.

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Regulation of nitric oxide production from macrophages by lipopolysaccharide and catecholamines

Cited by 103 publications

References 27 publications

Involvement of CB₁-receptors and β-adrenoceptors in the regional hemodynamic responses to lipopolysaccharide infusion in conscious rats

Involvement of CB₁-receptors and β-adrenoceptors in the regional hemodynamic responses to lipopolysaccharide infusion in conscious rats

Chronic β-Adrenergic Receptor Stimulation Induces Cardiac Apoptosis and Aggravates Myocardial Ischemia/Reperfusion Injury by Provoking Inducible Nitric-Oxide Synthase-Mediated Nitrative Stress

Modulatory Effects of 6‐Carboxymethylthiopurine on Activated Murine Macrophages

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Regulation of nitric oxide production from macrophages by lipopolysaccharide and catecholamines

Cited by 103 publications

References 27 publications

Involvement of CB1-receptors and β-adrenoceptors in the regional hemodynamic responses to lipopolysaccharide infusion in conscious rats

Involvement of CB1-receptors and β-adrenoceptors in the regional hemodynamic responses to lipopolysaccharide infusion in conscious rats

Chronic β-Adrenergic Receptor Stimulation Induces Cardiac Apoptosis and Aggravates Myocardial Ischemia/Reperfusion Injury by Provoking Inducible Nitric-Oxide Synthase-Mediated Nitrative Stress

Modulatory Effects of 6‐Carboxymethylthiopurine on Activated Murine Macrophages

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Involvement of CB₁-receptors and β-adrenoceptors in the regional hemodynamic responses to lipopolysaccharide infusion in conscious rats

Involvement of CB₁-receptors and β-adrenoceptors in the regional hemodynamic responses to lipopolysaccharide infusion in conscious rats