Browsing by Subject "leg"
Now showing 1 - 2 of 2
- Results Per Page
- Sort Options
Item Control of the Peripheral Vasculature During Exercise: Angiotensin II(2007-04-01) Brothers, Robert Matthew; Peter B. Raven; Michael Smith; Patricia GwirtzBrothers, 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.Item Interaction of Neural and Local Mechanisms in the Control of Skeletal Muscle Blood Flow(2003-12-01) Wray, David Walter; Michael L. SmithWray, David Walter, Interaction of Neural and Local Mechanisms in the Control of Skeletal Muscle Blood Flow. Doctor of Philosophy (Biomedical Science), December, 2003, 181 pp., 1 table, 19 illustrations, references, 139 titles. The current project sought to characterize the interaction of neural and local mechanisms of skeletal muscle blood flow control through exogenous and endogenous α-andrenoreceptor activation. We hypothesized that α1- and α2-adrenoreceptors in the human leg would exhibit differential distribution and responsiveness, and that unilateral knee-extensor exercise would attenuate α-adrenoreceptor-mediated vasoconstriction in an intensity-dependent manner. We also hypothesized that carotid baroreflex (CBR)-mediated sympathoexcitation would provoke less vasoconstriction during exercise than at rest. Intra-arterial infusion of phenylephrine (PE, α1-agonist) or BHT-933 (α2-agonist) reduced femoral blood flow (FBF) by approximately 60% at rest, but during exercise (27W) the degree of vasoconstriction evoked by PE and BHT was significantly reduced. During ramped (7W-37W) exercise, BHT did not reduce FBF at any intensity, while some degree of PE-induced vasoconstriction was evident at all but the highest exercise intensity. Using sinusoidal neck pressure, CBR-mediated changes in heart rate (HR), arterial blood pressure (ABP) muscle sympathetic nerve activity (MSNA), FBF, and tissue oxygenation (TOm) were seen at rest. During 7w exercise, CBR-mediated control of ABP, FBF, and Tom was attenuated. We conclude that exercise attenuates α-adrenergic responsiveness to exogenous and endogenous activation to ensure sufficient muscle blood flow while maintaining systemic ABP homeostasis.