University of Louisville

Poster Title

The Role of Antioxidant Tempol on Endothelial-Mediated Vascular Responsiveness

Institution

University of Louisville

Abstract

Hypertension is a major health problem in the United States, where more than 50 million people (1 in 4 adults) have the condition. Research suggests that hypertension development creates oxidative stress in the body forming harmful reactive oxygen species attacking the microvasculature, particularly the endothelium. Endothelium produces nitric oxide, essential in smooth muscle relaxation. The use of antioxidants such as Tempol neutralize these free radicals therefore restoring relaxation. We hypothesize that there is a decrease in aortic endothelial mediated relaxation with hypertension development and these alterations are due to oxidative stress. The objective of this study was to develop a protocol that would effectively help us investigate the presence of oxidative stress in the aorta of the mouse. Vascular function was determined in thoracic aorta segments of female wild-type mice exposed to vasoactive agents. In vitro studies involved dose responses to acetylcholine (ACH), sodium nitroprusside (SNP) and phenylephrine (PHE). Results indicate that endothelial dependent relaxation could be decreased in the presence of Tempol. The contraction response to PHE didn't appear to be affected with or without Tempol. Aortic relaxation to SNP appears to be increased in comparison to ACH. The results could also suggest that endothelial cells of the aorta were damaged during the aortic ring preparation. Therefore, we are currently conducting more experiments to continue our investigation of the role of Tempol endothelial-mediated vascular responsiveness.

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The Role of Antioxidant Tempol on Endothelial-Mediated Vascular Responsiveness

Hypertension is a major health problem in the United States, where more than 50 million people (1 in 4 adults) have the condition. Research suggests that hypertension development creates oxidative stress in the body forming harmful reactive oxygen species attacking the microvasculature, particularly the endothelium. Endothelium produces nitric oxide, essential in smooth muscle relaxation. The use of antioxidants such as Tempol neutralize these free radicals therefore restoring relaxation. We hypothesize that there is a decrease in aortic endothelial mediated relaxation with hypertension development and these alterations are due to oxidative stress. The objective of this study was to develop a protocol that would effectively help us investigate the presence of oxidative stress in the aorta of the mouse. Vascular function was determined in thoracic aorta segments of female wild-type mice exposed to vasoactive agents. In vitro studies involved dose responses to acetylcholine (ACH), sodium nitroprusside (SNP) and phenylephrine (PHE). Results indicate that endothelial dependent relaxation could be decreased in the presence of Tempol. The contraction response to PHE didn't appear to be affected with or without Tempol. Aortic relaxation to SNP appears to be increased in comparison to ACH. The results could also suggest that endothelial cells of the aorta were damaged during the aortic ring preparation. Therefore, we are currently conducting more experiments to continue our investigation of the role of Tempol endothelial-mediated vascular responsiveness.