Browsing by Subject "Carotid baroreflex"
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Item Carotid Baroreflex of Leg Vasculature(2004-07-01) Keller, David Melvin; Peter A. Raven; H. Fred Downey; Patricia A. GwirtzKeller, David Melvin, Carotid Baroreflex Control of Leg Vasculature. Doctor of Philosophy (Biomedical Science), July 2004; 110 pp; 5 tables; 10 figures; bibliography. The carotid baroreflex (CBR) exerts control of arterial blood pressure primarily as a result of changes in total vascular conductance. In humans, understanding CBR control of the vasculature supplying a given vascular bed, such as the leg, remains unclear. Furthermore, it appears that metabolic attenuation of sympathetic vasoconstriction may modulate the CBR of the vasculature supplying contracting skeletal muscle during exercise. However, the balance between baroreflex-mediated vasoconstriction and the mechanisms responsible for the metabolic attenuation has not been fully elucidated. Therefore, the purpose of the investigations within this dissertation was to: i) explain CBR control of leg vascular conductance (LVC) and the relationship between changes in LVC and muscle sympathetic nerve activity at rest and during one-legged knee extension exercise, ii) examine the CBR control of the vasculature supplying an exercising leg and a non-exercising leg during exercise, and iii) demonstrate the role of the ATP-sensitive potassium channel in contributing to the metabolic attenuation of CBR-mediated vasoconstriction in the vasculature supplying contracting skeletal muscle. In the first investigation, we demonstrated: i) the stimulus response relationships for CBR control of LVC and MSNA at rest and during two intensities of one-legged knee extension exercise; ii) that CBR control of LVC was preserved during exercise; iii) that the attenuation of CBR-mediated vasoconstriction was no different between 7W and 25W exercise in the vasculature supplying an exercising leg; and iv) that the contribution of changes in LVC to CBR changes in mean arterial pressure was no different from rest to exercise in both the exercising leg and the non-exercising leg. In the second investigation, we examined the role of the ATP-sensitive potassium channel in modulating sympathetically-mediated vasoconstriction at rest and during exercise in the vasculature supplying an exercising leg and a non-exercising leg. The attenuated vasoconstrictor response to the carotid baroreceptor stimulated hypotension observed in the vasculature supplying an exercising leg was partially restored two to four hours after the oral ingestion of glyburide (5mg). This finding indicates that ATP-sensitive potassium channel activation plays a primary role in the effects of functional sympatholysis during leg exercise in humans. We further demonstrated that CBR control of MAP was not altered by oral glyburide administration in healthy subjects.Item Regulation of Carotid Baroreflex Resetting During Arm Exercise(1999-06-01) Querry, Ross G.; Peter B. Raven; Patricia Gwirtz; Michael SmithQuerry, Ross G., Regulation of Carotid Baroreflex Resetting during Arm Exercise. Doctor of Philosophy (Biomedical Sciences), June 1999, 100 pp., 4 tables, 12 figures, bibliography, 56 titles. Cardiovascular responses to exercise are modulated by the integration of the central nervous system and afferent information from arterial baroreflexes and working skeletal muscle. Investigations have shown that during exercise, the carotid baroreflex (CBR) is reset in proportion to the exercise intensity. The role of the central nervous system contribution to the CBR resetting has not been elucidated. Investigations of CBR function in the animal model consistently report CBR variables such as maximal gain that are different than those reported in humans. These discrepancies may be due in part to methodological limitations in the neck pressure/neck suction (NP-NS) technique used to investigate the isolated CBR function in humans. To accurately examine the internal stimulus from the NP-NS maneuver, subjects were instrumented with a percutaneous catheter to record tissue pressure at the carotid sinus during five-second and rapid pulse NP-NS protocols. Carotid baroreflex function curves were analyzed with and without transmission correction of the carotid sinus pressure (CSP). Results indicated that positive pressure was more fully transmitted (~83%) than negative pressure (~65%) during the five-second-pulse, but not the rapid pulse protocol. Correction of the CSP in either protocol resulted in significant increases in CBR maximal gain and threshold and a reduced saturation pressure. These methodological refinements were then utilized to investigate the role of central command on CBR function during exercise. Subjects performed static and rhythmic handgrip exercise before and after regional anesthesia. Carotid baroreflex curves were analyzed at rest and during exercise before and after blockade at the same absolute workload. Muscle weakness from the blockade required an increased effort to maintain control tension. Heart rate, arterial pressure and perceived exertion during exercise were increased following blockade. During control exercise the CBR function curves were reset upward and rightward compared to rest with a further parallel shift during exercise with blockade. The operating point of the CBR was reset along with the centering point, but did not show the divergence toward the threshold pressure that had been previously described during dynamic exercise. The results support the proposal that central command was a primary mechanism for the resetting of the carotid baroreflex during exercise, but may not be the primary mechanism in the resetting of the operating point of the reflex.