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Down-regulation of ventricular nitric oxide generating system in chronic alcohol-treated hypertensive rats.
Cell Mol Biol (Noisy-le-grand). 2007 May 15; 53(4):32-7.CM

Abstract

Epidemiological studies show that low to moderate doses of alcohol consumption is beneficial to cardiac health. However, chronic high doses of alcohol ingestion cause cardiovascular complications including hypertension. The molecular and cellular mechanisms of chronic ethanol-induced increase in blood pressure (BP) are not completely understood. The purpose of this study was to investigate whether the increase in blood pressure following chronic ethanol exposure relates to cardiac endothelial nitric oxide levels and its generating system. Male Fisher rats were given 20% ethanol (4 g/kg, orally) through orogastric tube daily for 12 weeks and controls received 5% sucrose through orogastric tube daily for 12 weeks. The systolic, diastolic and mean BP was recorded through tail-cuff method. After 12 weeks, rats were sacrificed and heart dissected and left ventricle isolated and analyzed using enzyme linked immunosorbant assay (ELISA) and Western blotting. Results show that ethanol ingestion caused a significant increase in systolic, diastolic and mean BP (p<0.001) compared to control after 12 weeks. The levels of nitric oxide, its generating enzyme endothelial nitric oxide synthase (eNOS) protein expression and vascular endothelial growth factor (VEGF) gene (mRNA) and protein expressions were significantly down-regulated in the endothelium of left ventricles of ethanol-treated rats compared to controls. It is concluded that chronic ethanol ingestion causes an increase in blood pressure in rats via endothelial oxidative injury and the down-regulation of nitric oxide generating system in the left ventricles.

Authors+Show Affiliations

Department of Physiology, Pharmacology and Toxicology, Ponce School of Medicine, Ponce, Puerto Rico. khusain@psm.eduNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

17531158

Citation

Husain, K, et al. "Down-regulation of Ventricular Nitric Oxide Generating System in Chronic Alcohol-treated Hypertensive Rats." Cellular and Molecular Biology (Noisy-le-Grand, France), vol. 53, no. 4, 2007, pp. 32-7.
Husain K, Vazquez-Ortiz M, Lalla J. Down-regulation of ventricular nitric oxide generating system in chronic alcohol-treated hypertensive rats. Cell Mol Biol (Noisy-le-grand). 2007;53(4):32-7.
Husain, K., Vazquez-Ortiz, M., & Lalla, J. (2007). Down-regulation of ventricular nitric oxide generating system in chronic alcohol-treated hypertensive rats. Cellular and Molecular Biology (Noisy-le-Grand, France), 53(4), 32-7.
Husain K, Vazquez-Ortiz M, Lalla J. Down-regulation of Ventricular Nitric Oxide Generating System in Chronic Alcohol-treated Hypertensive Rats. Cell Mol Biol (Noisy-le-grand). 2007 May 15;53(4):32-7. PubMed PMID: 17531158.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Down-regulation of ventricular nitric oxide generating system in chronic alcohol-treated hypertensive rats. AU - Husain,K, AU - Vazquez-Ortiz,M, AU - Lalla,J, Y1 - 2007/05/15/ PY - 2006/10/27/received PY - 2006/11/15/accepted PY - 2007/5/29/pubmed PY - 2007/8/8/medline PY - 2007/5/29/entrez SP - 32 EP - 7 JF - Cellular and molecular biology (Noisy-le-Grand, France) JO - Cell Mol Biol (Noisy-le-grand) VL - 53 IS - 4 N2 - Epidemiological studies show that low to moderate doses of alcohol consumption is beneficial to cardiac health. However, chronic high doses of alcohol ingestion cause cardiovascular complications including hypertension. The molecular and cellular mechanisms of chronic ethanol-induced increase in blood pressure (BP) are not completely understood. The purpose of this study was to investigate whether the increase in blood pressure following chronic ethanol exposure relates to cardiac endothelial nitric oxide levels and its generating system. Male Fisher rats were given 20% ethanol (4 g/kg, orally) through orogastric tube daily for 12 weeks and controls received 5% sucrose through orogastric tube daily for 12 weeks. The systolic, diastolic and mean BP was recorded through tail-cuff method. After 12 weeks, rats were sacrificed and heart dissected and left ventricle isolated and analyzed using enzyme linked immunosorbant assay (ELISA) and Western blotting. Results show that ethanol ingestion caused a significant increase in systolic, diastolic and mean BP (p<0.001) compared to control after 12 weeks. The levels of nitric oxide, its generating enzyme endothelial nitric oxide synthase (eNOS) protein expression and vascular endothelial growth factor (VEGF) gene (mRNA) and protein expressions were significantly down-regulated in the endothelium of left ventricles of ethanol-treated rats compared to controls. It is concluded that chronic ethanol ingestion causes an increase in blood pressure in rats via endothelial oxidative injury and the down-regulation of nitric oxide generating system in the left ventricles. SN - 1165-158X UR - https://www.unboundmedicine.com/medline/citation/17531158/Down_regulation_of_ventricular_nitric_oxide_generating_system_in_chronic_alcohol_treated_hypertensive_rats_ L2 - https://medlineplus.gov/highbloodpressure.html DB - PRIME DP - Unbound Medicine ER -