Adrenergic receptors regulate macrophage secretion

Shen, Hong; Sha, Lei; Kennedy, John; Ou, Dawei

doi:10.1016/0192-0561(94)90045-0

Cited by 28 publications

(10 citation statements)

References 21 publications

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“…Therefore, our study could not rule out that the endotoxaemia-induced ileus might have been ameliorated by altering inflammatory reactions or haemodynamics in response to yohimbine. 29 31 40 Yohimbine has been approved by the Food and Drug Administration for clinical use in the treatment of erectile dysfunction. 41 In addition, clinical trials are ongoing to test the effect of yohimbine in colon transit for treating constipation.…”

Section: Discussionmentioning

confidence: 99%

The α 2 -adrenergic receptor antagonist yohimbine improves endotoxin-induced inhibition of gastrointestinal motility in mice

Hamano

Inada

Iwata

et al. 2007

British Journal of Anaesthesia

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Section: Discussionmentioning

confidence: 99%

The α 2 -adrenergic receptor antagonist yohimbine improves endotoxin-induced inhibition of gastrointestinal motility in mice

Hamano

Inada

Iwata

et al. 2007

British Journal of Anaesthesia

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“…Similarly, adrenergic agents decrease TNF production during human endotoxemia [188], as well as decrease macrophage superoxide and NO release [189]. Thus, ischemia and reperfusion induce myocardial damage which is likely mediated, in part, by destructive inflammation.…”

Section: Preconditioningmentioning

confidence: 99%

Role of TNF in Mediating Renal Insufficiency Following Cardiac Surgery: Evidence of a Postbypass Cardiorenal Syndrome

Meldrum¹,

Donnahoo²

1999

Journal of Surgical Research

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“…Catecholamines have important regulatory functions on macrophages as well as on B and T cells (11)(12)(13)(14)(15). For example, in vitro experiments show that ␣ -adrenergic stimulation of macrophages leads to increased TNF-␣ expression (16,17), while ␤ -adrenergic stimulation, through an increase in cAMP, inhibits the production of cytokines such as TNF-␣ , IL-1 ␤ , and IL-6 (18)(19)(20)(21).…”

Section: Introductionmentioning

confidence: 99%

Hemorrhage increases cytokine expression in lung mononuclear cells in mice: involvement of catecholamines in nuclear factor-kappaB regulation and cytokine expression.

et al. 1997

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The expression of proinflammatory and immunoregulatory cytokines rapidly increases in the lungs after hemorrhage, and such alterations contribute to the frequent development of acute inflammatory lung injury in this setting. Blood loss also produces elevations in catecholamine concentrations in the pulmonary and systemic circulation. In the present experiments, we used ␣ -and ␤ -adrenergic receptor blockade to examine in vivo interactions between hemorrhage-induced adrenergic stimulation and pulmonary cytokine expression. Treatment of mice with the ␣ -adrenergic receptor antagonist phentolamine prevented not only the elevation in mRNA levels of IL-1 ␤ , TNF-␣ , and TGF-␤ 1, the increase in IL-1 ␤ protein, but also the activation of nuclear factor (NF)-B and cyclic AMP response element binding protein, which occurred in lung cells of untreated animals during the first hour after hemorrhage. In contrast, treatment before hemorrhage with the ␤ -adrenergic receptor antagonist propranolol was associated with increases in mRNA levels for IL-1 ␤ , TNF-␣ , and TGF-␤ 1, which were greater than those present in untreated hemorrhaged mice, and did not prevent hemorrhage-associated increases in lung IL-1 ␤ protein. Treatment with propranolol prevented hemorrhageinduced phosphorylation of cyclic AMP response element binding protein, but increased hemorrhage-associated activation of NF-B. These results demonstrate that hemorrhage initially increases pulmonary cytokine expression through ␣ -but not ␤ -adrenergic stimulation, and suggest that such ␣ -adrenergic-mediated effects occur through activation of the transcriptional regulatory factor NF-B. ( J. Clin. Invest. 1997. 99:1516-1524.)

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Adrenergic receptors regulate macrophage secretion

Cited by 28 publications

References 21 publications

The α 2 -adrenergic receptor antagonist yohimbine improves endotoxin-induced inhibition of gastrointestinal motility in mice

The α 2 -adrenergic receptor antagonist yohimbine improves endotoxin-induced inhibition of gastrointestinal motility in mice

Role of TNF in Mediating Renal Insufficiency Following Cardiac Surgery: Evidence of a Postbypass Cardiorenal Syndrome

Hemorrhage increases cytokine expression in lung mononuclear cells in mice: involvement of catecholamines in nuclear factor-kappaB regulation and cytokine expression.

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