Tags

Type your tag names separated by a space and hit enter

Chronic ethanol ingestion induces aortic inflammation/oxidative endothelial injury and hypertension in rats.
Hum Exp Toxicol. 2011 Aug; 30(8):930-9.HE

Abstract

The study aim was to investigate the relationship of chronic ethanol-induced inflammation leading to vascular endothelial injury and elevation of blood pressure (BP) in a rat model. Male Fisher rats were divided into two groups of six animals each and treated as follows: (1) Control (5% sucrose, orally) daily for 12 weeks and (2) 20% ethanol (4 g kg(-1), orally) daily for 12 weeks. The mean arterial blood pressure was recorded every week. The animals were anesthetized with pentobarbital after 12 weeks; thoracic aorta were isolated and analyzed for aortic reactivity response, inflammatory mediators, oxidant/antioxidant enzyme protein expression and endothelial nitric oxide-generating system. The results show that the mean BP was significantly elevated 12 weeks after ethanol ingestion. The increased BP was related to increased aortic inflammation (tumor necrosis factor [TNF]-α; nitric oxide synthase [iNOS], COX-2 and MCP-1 protein expression) and elevated angiotensin II levels in alcohol-treated group compared to control. Aortic Nicotinamide adenine dinucleotide phosphate reduced (NADPH) oxidase activity, membrane and cytosolic subunits p22(phox) and p47(phox) expression and Mn-SOD activity and protein expression significantly increased, whereas nitric oxide (NO), endothelial NO synthase (eNOS), vascular endothelial growth factor (VEGF)-A and CuZn-SOD activity and protein expression significantly decreased in alcohol-treated group compared to control. The acetylcholine-mediated vasorelaxation response was depressed in the aorta of ethanol-treated rats compared to control. In conclusion, chronic ethanol-induced elevation in BP is related to increased aortic inflammation, elevated angiotensin II levels, induction of NADPH oxidase causing endothelial injury, depletion of CuZn-SOD, down-regulation of endothelial NO generating system and impaired vascular relaxation in rats.

Authors+Show Affiliations

Department of Physiology, Pharmacology and Toxicology, Ponce School of Medicine, Ponce, PR, USA. kazimhusain@hotmail.comNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural

Language

eng

PubMed ID

20921064

Citation

Husain, Kazim, et al. "Chronic Ethanol Ingestion Induces Aortic Inflammation/oxidative Endothelial Injury and Hypertension in Rats." Human & Experimental Toxicology, vol. 30, no. 8, 2011, pp. 930-9.
Husain K, Ferder L, Ansari RA, et al. Chronic ethanol ingestion induces aortic inflammation/oxidative endothelial injury and hypertension in rats. Hum Exp Toxicol. 2011;30(8):930-9.
Husain, K., Ferder, L., Ansari, R. A., & Lalla, J. (2011). Chronic ethanol ingestion induces aortic inflammation/oxidative endothelial injury and hypertension in rats. Human & Experimental Toxicology, 30(8), 930-9. https://doi.org/10.1177/0960327110384520
Husain K, et al. Chronic Ethanol Ingestion Induces Aortic Inflammation/oxidative Endothelial Injury and Hypertension in Rats. Hum Exp Toxicol. 2011;30(8):930-9. PubMed PMID: 20921064.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Chronic ethanol ingestion induces aortic inflammation/oxidative endothelial injury and hypertension in rats. AU - Husain,Kazim, AU - Ferder,Leon, AU - Ansari,Rais A, AU - Lalla,Jainarine, Y1 - 2010/10/04/ PY - 2010/10/6/entrez PY - 2010/10/6/pubmed PY - 2011/12/13/medline SP - 930 EP - 9 JF - Human & experimental toxicology JO - Hum Exp Toxicol VL - 30 IS - 8 N2 - The study aim was to investigate the relationship of chronic ethanol-induced inflammation leading to vascular endothelial injury and elevation of blood pressure (BP) in a rat model. Male Fisher rats were divided into two groups of six animals each and treated as follows: (1) Control (5% sucrose, orally) daily for 12 weeks and (2) 20% ethanol (4 g kg(-1), orally) daily for 12 weeks. The mean arterial blood pressure was recorded every week. The animals were anesthetized with pentobarbital after 12 weeks; thoracic aorta were isolated and analyzed for aortic reactivity response, inflammatory mediators, oxidant/antioxidant enzyme protein expression and endothelial nitric oxide-generating system. The results show that the mean BP was significantly elevated 12 weeks after ethanol ingestion. The increased BP was related to increased aortic inflammation (tumor necrosis factor [TNF]-α; nitric oxide synthase [iNOS], COX-2 and MCP-1 protein expression) and elevated angiotensin II levels in alcohol-treated group compared to control. Aortic Nicotinamide adenine dinucleotide phosphate reduced (NADPH) oxidase activity, membrane and cytosolic subunits p22(phox) and p47(phox) expression and Mn-SOD activity and protein expression significantly increased, whereas nitric oxide (NO), endothelial NO synthase (eNOS), vascular endothelial growth factor (VEGF)-A and CuZn-SOD activity and protein expression significantly decreased in alcohol-treated group compared to control. The acetylcholine-mediated vasorelaxation response was depressed in the aorta of ethanol-treated rats compared to control. In conclusion, chronic ethanol-induced elevation in BP is related to increased aortic inflammation, elevated angiotensin II levels, induction of NADPH oxidase causing endothelial injury, depletion of CuZn-SOD, down-regulation of endothelial NO generating system and impaired vascular relaxation in rats. SN - 1477-0903 UR - https://www.unboundmedicine.com/medline/citation/20921064/Chronic_ethanol_ingestion_induces_aortic_inflammation/oxidative_endothelial_injury_and_hypertension_in_rats_ L2 - https://journals.sagepub.com/doi/10.1177/0960327110384520?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -