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Evidence for the involvement of NADPH oxidase in ischemia/reperfusion-induced gastric damage via angiotensin II.
J Physiol Pharmacol. 2010 Apr; 61(2):171-9.JP

Abstract

Reactive oxygen species are known to be derived from NADPH oxidase in several tissues. Angiotensin II was suggested to be involved in the activation of NADPH oxidase; however, its role in the gastric mucosa is unclear. We examined the roles of angiotensin II receptor and NADPH oxidase in ischemia/reperfusion-induced gastric damage in rats. Under urethane anesthesia, male Sprague-Dawley rat stomachs were mounted in an ex-vivo chamber, had 100 mM HCl applied to them, and then a catheter was passed through the femoral vein. Ischemia/reperfusion was accompanied by blood collection and reperfusion through the catheter. Losartan, candesartan, valsartan, which are AT1 receptor blockers (ARB); PD123319, an AT2 receptor blocker; enalapril, an ACE inhibitor; or diphenylene iodonium, a NADPH oxidase inhibitor, was given i.v. 10 mins, and beta-NADPH, a NADPH oxidase substrate, was given i.v. 5 mins before reperfusion. The gastric damage by ischemia/reperfusion was attenuated by treatment with any of ARB or enalapril, but was not affected by PD123319. The increase in gastric H(2)O(2) production and microvascular permeability by ischemia/reperfusion was also suppressed by treatment with any of ARB or enalapril. In rat gastric mucosa, the NADPH oxidase subunit p47(phox) was detected. Additionally, diphenylene iodonium had similar effects to ARB against ischemia/reperfusion-caused gastric damage, increased H(2)O(2) production, and microvascular permeability. Ischemia/reperfusion activated NADPH oxidase in the gastric mucosa, and the activation was significantly attenuated by treatment with losartan or diphenylene iodonium. These results suggest that ischemia/reperfusion generated reactive oxygen species are derived from NADPH oxidase activation via AT1 receptor in rat stomachs.

Authors+Show Affiliations

Department of Pharmacotherapeutics, Clinical Pharmacy, Doshisha Women's College of Liberal Arts, Kodo, Kyotanabe, Kyoto, Japan. anakagir@dwc.doshisha.ac.jpNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

20436217

Citation

Nakagiri, A, et al. "Evidence for the Involvement of NADPH Oxidase in Ischemia/reperfusion-induced Gastric Damage Via Angiotensin II." Journal of Physiology and Pharmacology : an Official Journal of the Polish Physiological Society, vol. 61, no. 2, 2010, pp. 171-9.
Nakagiri A, Sunamoto M, Takeuchi K, et al. Evidence for the involvement of NADPH oxidase in ischemia/reperfusion-induced gastric damage via angiotensin II. J Physiol Pharmacol. 2010;61(2):171-9.
Nakagiri, A., Sunamoto, M., Takeuchi, K., & Murakami, M. (2010). Evidence for the involvement of NADPH oxidase in ischemia/reperfusion-induced gastric damage via angiotensin II. Journal of Physiology and Pharmacology : an Official Journal of the Polish Physiological Society, 61(2), 171-9.
Nakagiri A, et al. Evidence for the Involvement of NADPH Oxidase in Ischemia/reperfusion-induced Gastric Damage Via Angiotensin II. J Physiol Pharmacol. 2010;61(2):171-9. PubMed PMID: 20436217.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Evidence for the involvement of NADPH oxidase in ischemia/reperfusion-induced gastric damage via angiotensin II. AU - Nakagiri,A, AU - Sunamoto,M, AU - Takeuchi,K, AU - Murakami,M, PY - 2009/01/05/received PY - 2010/03/19/accepted PY - 2010/5/4/entrez PY - 2010/5/4/pubmed PY - 2010/8/4/medline SP - 171 EP - 9 JF - Journal of physiology and pharmacology : an official journal of the Polish Physiological Society JO - J Physiol Pharmacol VL - 61 IS - 2 N2 - Reactive oxygen species are known to be derived from NADPH oxidase in several tissues. Angiotensin II was suggested to be involved in the activation of NADPH oxidase; however, its role in the gastric mucosa is unclear. We examined the roles of angiotensin II receptor and NADPH oxidase in ischemia/reperfusion-induced gastric damage in rats. Under urethane anesthesia, male Sprague-Dawley rat stomachs were mounted in an ex-vivo chamber, had 100 mM HCl applied to them, and then a catheter was passed through the femoral vein. Ischemia/reperfusion was accompanied by blood collection and reperfusion through the catheter. Losartan, candesartan, valsartan, which are AT1 receptor blockers (ARB); PD123319, an AT2 receptor blocker; enalapril, an ACE inhibitor; or diphenylene iodonium, a NADPH oxidase inhibitor, was given i.v. 10 mins, and beta-NADPH, a NADPH oxidase substrate, was given i.v. 5 mins before reperfusion. The gastric damage by ischemia/reperfusion was attenuated by treatment with any of ARB or enalapril, but was not affected by PD123319. The increase in gastric H(2)O(2) production and microvascular permeability by ischemia/reperfusion was also suppressed by treatment with any of ARB or enalapril. In rat gastric mucosa, the NADPH oxidase subunit p47(phox) was detected. Additionally, diphenylene iodonium had similar effects to ARB against ischemia/reperfusion-caused gastric damage, increased H(2)O(2) production, and microvascular permeability. Ischemia/reperfusion activated NADPH oxidase in the gastric mucosa, and the activation was significantly attenuated by treatment with losartan or diphenylene iodonium. These results suggest that ischemia/reperfusion generated reactive oxygen species are derived from NADPH oxidase activation via AT1 receptor in rat stomachs. SN - 1899-1505 UR - https://www.unboundmedicine.com/medline/citation/20436217/Evidence_for_the_involvement_of_NADPH_oxidase_in_ischemia/reperfusion_induced_gastric_damage_via_angiotensin_II_ L2 - http://www.jpp.krakow.pl/journal/archive/04_10/pdf/171_04_10_article.pdf DB - PRIME DP - Unbound Medicine ER -