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Expressions of inducible nitric oxide synthase and cyclooxygenase-2 in gastric ischemia-reperfusion: role of angiotensin II.
J Surg Res. 2010 Jun 01; 161(1):126-33.JS

Abstract

BACKGROUND

Angiotensin II contributes to the pathogenesis of inflammation induced by ischemia-reperfusion (I/R) in various organs. Angiotensin II increases vascular permeability that initiates the inflammatory process and leads to the migration of inflammatory cells into the tissue. The aim of the present study was to investigate the effect of angiotensin II on ischemia-reperfusion induced expressions of inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2) in rat stomachs exposed to ischemia-reperfusion.

METHODS

Wistar rats were randomly separated into five groups: sham operated, I/R, I/R plus candesartan (an AT1 receptor antagonist), I/R plus PD123319 (an AT2 receptor antagonist), and I/R plus captopril (an angiotensin-converting enzyme inhibitor). Candesartan (1mg/kg/d), PD123319 (3mg/kg/d), and captopril (20mg/kg/d) were given subcutaneously twice a day for 5 d before I/R. The rats were submitted to gastric ischemia by clamping the celiac artery for 30min followed by 24h reperfusion.

RESULTS

Candesartan decreased the neutrophil accumulation, iNOS expression, and increased NOx level, COX-2 expression in the gastric tissue exposed to I/R compared with I/R group. PD123319 did not change the neutrophil accumulation, iNOS expression, PGE(2), or NOx levels, but increased the expression of COX-2 in the gastric tissue exposed to I/R. However, captopril did not play any role in I/R induced change in gastric mucosa.

CONCLUSIONS

The results suggest that Angiotensin II via angiotensin II type 1 receptor increases the accumulation of neutrophils and iNOS expression and plays a significant role in mediating inflammation in gastric mucosa exposed to I/R.

Authors+Show Affiliations

Department of Physiology, Akdeniz University, Faculty of Medicine, Antalya, Turkey.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

19959193

Citation

Gemici, Burcu, et al. "Expressions of Inducible Nitric Oxide Synthase and Cyclooxygenase-2 in Gastric Ischemia-reperfusion: Role of Angiotensin II." The Journal of Surgical Research, vol. 161, no. 1, 2010, pp. 126-33.
Gemici B, Tan R, Ongüt G, et al. Expressions of inducible nitric oxide synthase and cyclooxygenase-2 in gastric ischemia-reperfusion: role of angiotensin II. J Surg Res. 2010;161(1):126-33.
Gemici, B., Tan, R., Ongüt, G., & Izgüt-Uysal, V. N. (2010). Expressions of inducible nitric oxide synthase and cyclooxygenase-2 in gastric ischemia-reperfusion: role of angiotensin II. The Journal of Surgical Research, 161(1), 126-33. https://doi.org/10.1016/j.jss.2009.07.018
Gemici B, et al. Expressions of Inducible Nitric Oxide Synthase and Cyclooxygenase-2 in Gastric Ischemia-reperfusion: Role of Angiotensin II. J Surg Res. 2010 Jun 1;161(1):126-33. PubMed PMID: 19959193.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Expressions of inducible nitric oxide synthase and cyclooxygenase-2 in gastric ischemia-reperfusion: role of angiotensin II. AU - Gemici,Burcu, AU - Tan,Ruken, AU - Ongüt,Gözde, AU - Izgüt-Uysal,V Nimet, Y1 - 2009/08/12/ PY - 2008/09/25/received PY - 2009/07/09/revised PY - 2009/07/12/accepted PY - 2009/12/5/entrez PY - 2009/12/5/pubmed PY - 2010/5/21/medline SP - 126 EP - 33 JF - The Journal of surgical research JO - J Surg Res VL - 161 IS - 1 N2 - BACKGROUND: Angiotensin II contributes to the pathogenesis of inflammation induced by ischemia-reperfusion (I/R) in various organs. Angiotensin II increases vascular permeability that initiates the inflammatory process and leads to the migration of inflammatory cells into the tissue. The aim of the present study was to investigate the effect of angiotensin II on ischemia-reperfusion induced expressions of inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2) in rat stomachs exposed to ischemia-reperfusion. METHODS: Wistar rats were randomly separated into five groups: sham operated, I/R, I/R plus candesartan (an AT1 receptor antagonist), I/R plus PD123319 (an AT2 receptor antagonist), and I/R plus captopril (an angiotensin-converting enzyme inhibitor). Candesartan (1mg/kg/d), PD123319 (3mg/kg/d), and captopril (20mg/kg/d) were given subcutaneously twice a day for 5 d before I/R. The rats were submitted to gastric ischemia by clamping the celiac artery for 30min followed by 24h reperfusion. RESULTS: Candesartan decreased the neutrophil accumulation, iNOS expression, and increased NOx level, COX-2 expression in the gastric tissue exposed to I/R compared with I/R group. PD123319 did not change the neutrophil accumulation, iNOS expression, PGE(2), or NOx levels, but increased the expression of COX-2 in the gastric tissue exposed to I/R. However, captopril did not play any role in I/R induced change in gastric mucosa. CONCLUSIONS: The results suggest that Angiotensin II via angiotensin II type 1 receptor increases the accumulation of neutrophils and iNOS expression and plays a significant role in mediating inflammation in gastric mucosa exposed to I/R. SN - 1095-8673 UR - https://www.unboundmedicine.com/medline/citation/19959193/Expressions_of_inducible_nitric_oxide_synthase_and_cyclooxygenase_2_in_gastric_ischemia_reperfusion:_role_of_angiotensin_II_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0022-4804(09)00389-8 DB - PRIME DP - Unbound Medicine ER -