Control of the Peripheral Vasculature During Exercise: Angiotensin II

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dc.contributor.advisorPeter B. Raven
dc.contributor.committeeMemberMichael Smith
dc.contributor.committeeMemberPatricia Gwirtz
dc.creatorBrothers, Robert Matthew
dc.date.accessioned2019-08-22T21:33:52Z
dc.date.available2019-08-22T21:33:52Z
dc.date.issued2007-04-01
dc.date.submitted2013-06-27T15:00:08-07:00
dc.description.abstractBrothers, Robert Matthew, Control of the Peripheral Vasculature During Exercise Angiotesin II. Doctor of Philosophy (Biomedical Science), April 2007, 126 pp; 3 tables; 12 figures; bibliography. Control of the vasculature during exercise is balance between sympathetic vasoconstriction and metabolic vasodilation. There is an exercise intensity dependent reduction in vasoconstriction resulting in a shift towards vasodilation within “metabolically active” muscle and tissues, a phenomena known as “functional sympatholysis”. Previous studies investigating the alpha-receptors during exercise have used intra-arterial infusions of alpha-agonists. These studies indicate that alpha-receptor vasoconstrictionis completely attenuated during mild intensity exercise. When the alpha receptors are pharmacologically blocked the magnitude and onset of “functional sympatholysis” is not as drastic when compared to the agonist infusion studies. Intense exercise also activates the renin-angiotesin-system leading to production of angiotensin II (AngII), which increases exponentially at approximately 55% maximal oxygen uptake (55% VO2max). While the mechanisms of “functional sympatholysis” has been extensively studied less is known about the role of AngII in the control of the vasculature during exercise. Therefore, the purpose of the investigations within this dissertation was to: i)determine if alpha-1- blockade in an exercising human model will identify a greater maintenance of alpha-1 mediated vasoconstriction when compared to agonist infusion studies; ii) to determine if the metabolites produced within the active skeletal muscle will attenuate angiotensin II vasoconstriction; and iii) to determine if AngII vasoconstriction provides a greater percentage contribution to vascular tone as exercise intensity increases. We demonstrated that i) pharmacologic alpha-1-blockade identified a greater maintenance of alpha-1 vasoconstriction during moderately heavy exercise; and ii) this effect decreased as intensity increased in the exercising leg and increased with intensity in the non-exercising leg. In the second investigation we demonstrated that AngII and phenylephrine (PE) mediated vasoconstriction were attenuated to a similar degree during low and mild intensity exercise. In the third investigation we observed that AT1-receptor blockade; 1) attenuated the increases in MAP that occur during high-intensity exercise; ii) did not affect the vasculature in the exercising leg but; iii) we identified that AngII does partially control the vasculature in a “non-metabolically active” muscle group.
dc.format.mimetypeapplication/pdf
dc.identifier.urihttps://hdl.handle.net/20.500.12503/29426
dc.language.isoen
dc.provenance.legacyDownloads0
dc.subjectCardiology
dc.subjectCirculatory and Respiratory Physiology
dc.subjectExercise Science
dc.subjectKinesiology
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.subjectMusculoskeletal System
dc.subjectOther Kinesiology
dc.subjectVasculature control
dc.subjectsympathetic vasoconstriction
dc.subjectmetabolic vasodilation
dc.subjectperipheral vasculature
dc.subjectexercise
dc.subjectAngiotesin II
dc.subjectfunctional sympatholysis
dc.subjectrenin-angiotesin-system
dc.subjectAngII
dc.subjectexercise
dc.subjectleg
dc.subjectmuscle group
dc.titleControl of the Peripheral Vasculature During Exercise: Angiotensin II
dc.typeDissertation
dc.type.materialtext
thesis.degree.departmentGraduate School of Biomedical Sciences
thesis.degree.disciplineBiomedical Sciences
thesis.degree.grantorUniversity of North Texas Health Science Center at Fort Worth
thesis.degree.nameDoctor of Philosophy

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