Abstract |
Ischemia/reperfusion (I/R) damages gastric mucosa via reactive oxygen species (ROS) activity. ROS was reportedly produced through angiotensin II stimulation in tissues such as kidney, heart and brain. To determine whether AT1 receptor plays a role in gastric mucosal damage, we examined the effect of AT1 receptor blocker (ARB; losartan, candesartan, valsartan) on I/R-induced gastric injury in rats. I/R produced microscopic gastric hemorrhagic injury, and increased gastric microvascular permeability and H(2)O(2) production in rats. The mucosal lesions induced by I/R were attenuated by pretreatment of each ARB. The increase in microvascular permeability was suppressed by losartan pretreatment. Additionally, I/R-caused H(2)O(2) activation was not observed by pretreatment of losartan, candesartan and valsartan. These results suggest that angiotensin II stimulation via AT1 receptor and following ROS production in the stomach contribute to the pathogenesis of the gastric I/R injury.
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Authors | A Nakagiri, M Sunamoto, M Murakami |
Journal | Inflammopharmacology
(Inflammopharmacology)
Vol. 15
Issue 4
Pg. 171-4
(Aug 2007)
ISSN: 0925-4692 [Print] Switzerland |
PMID | 17701020
(Publication Type: Journal Article)
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Chemical References |
- Angiotensin II Type 1 Receptor Blockers
- Benzimidazoles
- Biphenyl Compounds
- Tetrazoles
- Angiotensin II
- Valsartan
- Hydrogen Peroxide
- Valine
- Losartan
- candesartan
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Topics |
- Angiotensin II
(physiology)
- Angiotensin II Type 1 Receptor Blockers
(pharmacology)
- Animals
- Benzimidazoles
(pharmacology)
- Biphenyl Compounds
- Capillary Permeability
(drug effects)
- Gastric Mucosa
(blood supply, drug effects, pathology)
- Hydrogen Peroxide
(metabolism)
- Losartan
(pharmacology)
- Male
- Microcirculation
(drug effects)
- Rats
- Rats, Sprague-Dawley
- Reperfusion Injury
(metabolism, pathology, prevention & control)
- Tetrazoles
(pharmacology)
- Valine
(analogs & derivatives, pharmacology)
- Valsartan
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