Jae Min Cho1,2, Yan-Ting Shiu3,4, J David Symons1,2, Timmy Lee5,6. 1. Department of Nutrition and Integrative Physiology and Molecular Medicine Program, University of Utah, Salt Lake City, Utah, USA. 2. Division of Endocrinology, Metabolism, and Diabetes, University of Utah, Salt Lake City, Utah, USA. 3. Veterans Affairs Medical Center, Section of Nephrology, Salt Lake City, Utah, USA. 4. Division of Nephrology and Hypertension, Department of Internal Medicine, University of Utah, Salt Lake City, Utah, USA. 5. Department of Medicine and Division of Nephrology, University of Alabama at Birmingham, Birmingham, Alabama, USA, txlee@uab.edu. 6. Veterans Affairs Medical Center, Section of Nephrology, Birmingham, Alabama, USA, txlee@uab.edu.
Abstract
INTRODUCTION: Impaired venous reactivity has potential to contribute to clinically significant pathologies such as arteriovenous fistula (AVF) maturation failure. Vascular segments commonly used in murine preclinical models of AVF include the carotid artery and external jugular vein. Detailed descriptions of isometric procedures to evaluate function of murine external jugular vein ex vivo have not been previously published. OBJECTIVE: To establish isometric procedures to measure naive murine external jugular vein reactivity ex vivo. METHODS: Vasomotor responses of external jugular veins and ipsilateral common carotid arteries from C57BL/6 mice were evaluated using isometric tension procedures. RESULTS: External jugular veins developed tension (p < 0.05) to potassium chloride and U-46619, but not to phenylephrine, whereas common carotid arteries responded to all 3 agents (p < 0.05). While maximal responses to acetylcholine (ACh) were similar between the venous and arterial segments, the dose required to achieve this value was lower (p < 0.05) in the artery versus vein. Nitric oxide synthase inhibition attenuated (p < 0.05) but did not abolish ACh-evoked vasorelaxation in both vascular segments, whereas cyclooxygenase blockade had no effect. Endothelium-independent vasorelaxation to sodium nitroprusside was similar in the artery and vein. CONCLUSION: Vasorelaxation and vasocontraction can be reliably assessed in the external jugular vein in C57BL/6 mice using isometric procedures.
INTRODUCTION: Impaired venous reactivity has potential to contribute to clinically significant pathologies such as arteriovenous fistula (AVF) maturation failure. Vascular segments commonly used in murine preclinical models of AVF include the carotid artery and external jugular vein. Detailed descriptions of isometric procedures to evaluate function of murine external jugular vein ex vivo have not been previously published. OBJECTIVE: To establish isometric procedures to measure naive murine external jugular vein reactivity ex vivo. METHODS: Vasomotor responses of external jugular veins and ipsilateral common carotid arteries from C57BL/6 mice were evaluated using isometric tension procedures. RESULTS: External jugular veins developed tension (p < 0.05) to potassium chloride and U-46619, but not to phenylephrine, whereas common carotid arteries responded to all 3 agents (p < 0.05). While maximal responses to acetylcholine (ACh) were similar between the venous and arterial segments, the dose required to achieve this value was lower (p < 0.05) in the artery versus vein. Nitric oxide synthase inhibition attenuated (p < 0.05) but did not abolish ACh-evoked vasorelaxation in both vascular segments, whereas cyclooxygenase blockade had no effect. Endothelium-independent vasorelaxation to sodium nitroprusside was similar in the artery and vein. CONCLUSION: Vasorelaxation and vasocontraction can be reliably assessed in the external jugular vein in C57BL/6 mice using isometric procedures.
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