A mechanistic study of β-adrenoceptor antagonists on ethanol-induced gastric damage

Kaan, Sheung K.; Mei, Qi; Cho, Chi H.

doi:10.1016/s0014-2999(96)00705-4

Cited by 8 publications

(6 citation statements)

References 17 publications

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“…Proinflammatory properties of epinephrine, reversible by ␤-receptor blockade or adrenal medullectomy, have been suggested by other in vivo models of inflammation (21)(22)(23)(24). However, both immunosuppressive and immunostimulatory effects of catecholamines have been described (25), with several recent in vitro studies suggesting that catecholamines suppress the release of proinflammatory cytokines (26)(27).…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, our models of CRH deficiency indicate that CRH largely masks this action of epinephrine. Possible mechanisms for epinephrine's effects include stimulation of neutrophil infiltration (24), increased capillary permeability by stimulation of kinin release (28), stimulation of cytokine release (29), adhesion of leukocytes to endothelial cells (30), and stimulation of peripheral nerve-mediated inflammatory signals (21).…”

Section: Discussionmentioning

confidence: 99%

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Corticotropin-releasing hormone deficiency unmasks the proinflammatory effect of epinephrine

Karalis

Kontopoulos

Muglia

et al. 1999

Proc. Natl. Acad. Sci. U.S.A.

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Traditionally, the adrenal gland has been considered an important endocrine component of the pathway to inhibit acute inflammation via hypothalamic corticotropin-releasing hormone (CRH)-mediated secretion of glucocorticoid. Immunoreactive CRH found in inflamed tissues is a potent proinflammatory factor. Using genetic and pharmacological models of CRH deficiency, we now show that CRH deficiency unmasks a major proinflammatory effect of epinephrine secreted from the adrenal medulla. Together, epinephrine and peripheral CRH stimulate inflammation, and glucocorticoid acts as a counterbalancing force in this regard. Our findings suggest that stimulation of the acute inflammatory response should be included with the other “fight-or-flight” actions of epinephrine.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Corticotropin-releasing hormone deficiency unmasks the proinflammatory effect of epinephrine

Karalis

Kontopoulos

Muglia

et al. 1999

Proc. Natl. Acad. Sci. U.S.A.

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“…Fig.3A shows that when terbutaline was administered IP at 5.0 mg/kg social withdrawal occurred similar to that seen with 1.5 mg/kg NE (30 ± 3% vs. 35 ± 7% at 0.5 h), (43 ± 11% vs. 51 ± 14% at 2 h), (67 ± 7% vs. 80 ± 1% at 4 h). Importantly, when the beta-2 antagonist butoxamine (Kaan et al, 1996; Junker et al, 2002) was administered IP at 5.0 mg/kg to mice just prior to NE injection (1.5 mg/kg), NE-dependent social withdrawal was completely blocked. Taken together these findings indicate that catecholamine-dependent social withdrawal is mediated by the beta-2 adrenergic receptor.…”

Section: Resultsmentioning

confidence: 99%

Blocking of beta-2 adrenergic receptors hastens recovery from hypoglycemia-associated social withdrawal

Park

Guest

Barnes

et al. 2008

Psychoneuroendocrinology

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Objective Hypoglycemia is associated with a variety of adverse behaviors including fatigue, confusion and social withdrawal. While these clinical symptoms are well characterized, the mechanism of their cause is not understood. Here we investigated how insulin-induced hypoglycemia causes social withdrawal. Research Design and Methods Male 8-12-wk-old C57BL/6J mice were injected intraperitoneally (IP) with or without and/or insulin, norepinephrine (NE) and epinephrine (Epi), terbutaline and butoxamine with subsequent measurement of blood glucose, social withdrawal and plasma catecholamines. Results Insulin generated (0.75 h post injection) significant hypoglycemia with blood glucose nadirs of 64 ± 4 and 48 ± 5 mg/dl for 0.8 and 1.2 units/kg of insulin, respectively. Insulin (0.8 or 1.2 units/kg) caused near total social withdrawal at 0.75 h with full recovery not occurring until 4 h (0.8 units/kg) or 8 h (1.2 units/kg) post insulin injection. Insulin also caused a marked elevation in plasma catecholamines. Basal 12 h fasting norepinephrine (NE) and epinephrine (Epi) were 287 ± 38 pg/ml and 350 ± 47 pg/ml, respectively. Insulin at 0.8 units/kg increased plasma NE and Epi to 994 ± 73 pg/ml and 1842 ± 473 pg/ml, respectively. Administration of exogenous NE or Epi caused social withdrawal similar in magnitude to insulin. Importantly, administration of the beta-2 adrenergic receptor agonist terbutaline also caused social withdrawal while administration of the beta-2 adrenergic receptor antagonist butoxamine blocked NE-induced social withdrawal. Finally, butoxamine blocked insulin-induced social withdrawal. Conclusions These data demonstrate that hypoglycemia-associated social withdrawal is dependent on catecholamines via a beta-2 receptor-mediated pathway.

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“…To the best of our knowledge, the current study is the first to report that nebivolol administration causes increase in gastric mucosal PGE 2 . However in support, Kaan et al (1996) reported that propranolol, a βadrenoceptor blocker, increases the PGE 2 levels in gastric mucosa which may explain its anti-ulcer effects. Further possible modes of gastroprotective action of nebivolol may be due to its possible antioxidant effects.…”

Section: Discussionmentioning

confidence: 94%

Nebivolol Ameliorates Indomethacin-Induced Gastric Ulcer in Adult Albino Rats: Role of Inducible Nitric Oxide Synthase

Allah

El-Din

2016

The Egyptian Journal of Forensic Sciences and Applied Toxicolog

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The effect of nebivolol (NBV), a third-generation selective β1antagonist, on indomethacin (IND)-induced gastric ulcer in rats was investigated. Thirty two male rats were used in this study, divided into four groups as follows: control group, IND ulcer-induced group, IND + NBV (1mg/kg/day, p.o.) group, and IND + NBV (5mg/kg/day, p.o.) group. Gastric ulcer was induced by a single injection of IND (30 mg/Kg, i.p.); NBV was administered for seven days prior to ulcer induction. At the end of the experiment, the stomach of each rat was removed for macroscopic examination and gastric ulcer scoring. The gastric mucosa was prepared for quantitative real-time polymerase chain reaction (qRT-PCR) and tissue homogenate preparation for biochemical study. Then, the remaining part was used for histopathological and immunohistochemical examination. Results showed that NBV significantly protected rats from indomethacin-induced gastric ulceration. There is a significant decreased in the mean ulcer number, score and index along with increased preventive index. Also, NBV significantly decreased the elevations of nitrite⁄nitrate, malondialdehyde, tumor necrosis factor-α, and interleukin-1beta in IND-treated rats. In addition, NBV significantly ameliorated the IND-induced reductions of glutathione level, glutathione peroxidase, superoxide dismutase, and catalase activities, and prostaglandin E 2. Moreover, histopathological, immunohistochemical analysis of inducible nitric oxide synthase (iNOS) and qRT-PCR for mRNA expression of iNOS gene:confirmed the biochemical results. It was concluded that NBV renders protection in IND-induced gastric ulceration in rats via maintenance of mucosal nitric oxide and prostaglandin E 2 , reducing oxidative stress and inflammatory responses.

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A mechanistic study of β-adrenoceptor antagonists on ethanol-induced gastric damage

Cited by 8 publications

References 17 publications

Corticotropin-releasing hormone deficiency unmasks the proinflammatory effect of epinephrine

Corticotropin-releasing hormone deficiency unmasks the proinflammatory effect of epinephrine

Blocking of beta-2 adrenergic receptors hastens recovery from hypoglycemia-associated social withdrawal

Nebivolol Ameliorates Indomethacin-Induced Gastric Ulcer in Adult Albino Rats: Role of Inducible Nitric Oxide Synthase

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