The role of nuclear factor-κB in the effect of angiotensin II in the paraventricular nucleus in protecting the gastric mucosa from ischemia-reperfusion injury in rats

Zhang, Yongmei; Wei, Er-qing; Hu, Xia; Qiao, Wei; Shi, Yue; Xu, Ming; Zhang, Jian‐Fu

doi:10.1007/s00535-008-2217-2

Cited by 13 publications

(6 citation statements)

References 49 publications

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“…microinjection of Ang II into the PVN inhibited mucosal injury in gastric ischemia-reperfusion induced ulcer model in a dose-dependent manner. The underlying mechanism is the increase of gastric blood flow, which effect turned to be mediated by central AT 1 receptors (Zhang et al, 2008). Moreover, reversal of the elevated mucosal level of NF-kappaB during gastric ischemia-reperfusion by Ang II may contribute to the Ang II-induced protection against injury (Zhang et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

Angiotensin II-induced activation of central AT1 receptors exerts endocannabinoid-mediated gastroprotective effect in rats

Gyires

Rónai

Zádori

et al. 2014

Molecular and Cellular Endocrinology

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The aim of the present study was to analyze whether angiotensin II via the endocannabinoid system can induce gastric mucosal protection, since transactivation of cannabinoid CB1 receptors by angiotensin AT1 receptor in CHO cells was described. Experimental ulcer was induced by acidified ethanol given orally in male Wistar rats, CB1(+/+) wild type and CB1(-/-) knock out mice. The compounds were administered intracerebroventricularly. It was found, that 1./ Angiotensin II inhibited the ethanol-induced gastric lesions (11.9-191 pmol); the effect of angiotensin II (191 pmol) was inhibited by the CB1 receptor inverse agonist AM 251 (1.8 nmol) and the inhibitor of diacylglycerol lipase (DAGL), tetrahydrolipstatin (0.2 nmol). 2./ Angiotensin II exerted gastroprotection in wild type, but not in CB1(-/-) mice. 3./ The gastroprotective effect of angiotensin II (191 pmol) was reduced by atropine (1 mg/kg i.v.) and bilateral cervical vagotomy. In conclusion, stimulation of central angiotensin AT1 receptors via activation of cannabinoid CB1 receptors induces gastroprotection in a DAGL-dependent and vagus-mediated mechanism.

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Section: Discussionmentioning

confidence: 99%

Angiotensin II-induced activation of central AT1 receptors exerts endocannabinoid-mediated gastroprotective effect in rats

Gyires

Rónai

Zádori

et al. 2014

Molecular and Cellular Endocrinology

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“…Several authors have reported that experimental gastric stress ulcerations may be prevented by the administra-tion of AT1 receptor blocking compounds both systemically and centrally (Pavel et al 2008, Zhang et al 2008a,b, Merai et al 2009). This mucosa protective effect has been proposed to be due to AT1 receptor mediated modulation of inflammatory factors, reduction of sympathetic neural activity and preservation of gastric mucosal blood perfusion (Pavel et al 2008).…”

Section: Mucosal Ulcerationsmentioning

confidence: 99%

The renin–angiotensin system and the gastrointestinal mucosa

Fändriks

2010

Acta Physiologica

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The gastrointestinal (GI) tract is fundamental for the intake of fluid and electrolytes and accommodates a large proportion of bodily hemodynamics and host defence systems. Despite that the renin-angiotensin system (RAS) is a prominent regulatory system for fluid and electrolyte homeostasis its impact on GI physiology is only little explored. Recent data indicate that RAS is well expressed and active in the GI tract although exact physiological roles are to be settled. There are several reports showing influences by RAS and its key mediator angiotensin II (AngII) on intestinal epithelial fluid and electrolyte transport and data are accumulating, suggesting involvement in GI mucosal inflammation and carcinogenesis. Of particular interest is the increasing amount of experimental support for the involvement of AngII formation and actions via the AngII subtype 1 (AT1) receptor in the pathogenesis and treatment of inflammatory bowel disease. The picture of RAS in the GI tract is, however, far from complete. Because RAS is an important application area for reno-cardiovascular diseases, a number of pharmacological agents as well as research technologies already exist and can in the future be used for GI research. A marked expansion of knowledge concerning the role of RAS in GI physiology and pathophysiology is to be expected.

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“…When NF-kB translocates to the nucleus, it activates the transcription genes related to inflammatory response. It has been reported that NF-kB is activated and translocated during I/R in the stomach [18]. Whether Ang II can regulate gastric ischemia reperfusion injury is not known for its possible molecular mechanisms.…”

Section: Introductionmentioning

confidence: 99%

Expressions of Inducible Nitric Oxide Synthase and Cyclooxygenase-2 in Gastric Ischemia-Reperfusion: Role of Angiotensin II

Gemici

Tan

Öngüt

et al. 2010

Journal of Surgical Research

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The role of nuclear factor-κB in the effect of angiotensin II in the paraventricular nucleus in protecting the gastric mucosa from ischemia-reperfusion injury in rats

Abstract: NF-kappaB plays a role in PVN Ang II-mediated protection against GI-R injury. These central effects of Ang II are mediated by AT1 receptors.

Cited by 13 publications

References 49 publications

Angiotensin II-induced activation of central AT1 receptors exerts endocannabinoid-mediated gastroprotective effect in rats

Angiotensin II-induced activation of central AT1 receptors exerts endocannabinoid-mediated gastroprotective effect in rats

The renin–angiotensin system and the gastrointestinal mucosa

Expressions of Inducible Nitric Oxide Synthase and Cyclooxygenase-2 in Gastric Ischemia-Reperfusion: Role of Angiotensin II

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