Browsing by Subject "aortic baroreflex"
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Item Arterial Baroreflex Control of Muscle Sympathetic Nerve Activity(2000-07-01) Fadel, Paul Joseph; Peter B. Raven; Michael Smith; Patricia GwirtzFadel, Paul Joseph, Jr., Arterial Baroreflex Control of Muscle Sympathetic Nerve Activity. Doctor of Philosophy (Biomedical Science), July 2000; 100 pp; 3 tables; 10 figures; bibliography. Arterial baroreflex control of sympathetic nerve activity is dependent on afferent nerve activity emanating from both the aortic and carotid baroreceptors. While several investigations have reported that the aortic baroreceptor reflex dominates in the baroreflex control of heart rate in humans, the role of carotid and the aortic baroreceptors in the control of sympathetic nerve activity remains unclear. In addition, the effect of exercise and long term endurance training on baroreflex-sympathetic nerve activity responses requires further definition. Therefore, the purpose of the investigations described within this dissertation was to: i) describe carotid baroreflex (CBR) control of muscle sympathetic nerve activity (MSNA) at rest and during exercise, ii) examine the relative contribution of the carotid and aortic baroreflexes to the overall arterial baroreflex control of MSNA during acute hypotension, and iii) determine the effect of fitness on arterial baroreflex control of MSNA. In the first investigation, we constructed stimulus-response relationships for CBR control of MSNA at rest and during dynamic arm cycling and demonstrated that carotid baroreflex control of MSNA was reset to function at the higher arterial pressures induced by exercise without a change in reflex sensitivity. Thus, we concluded that the carotid baroreflex control of MSNA was preserved during dynamic exercise. In the second investigation, acute hypotension was induced non-pharmacologically by releasing a unilateral arterial thigh cuff (300 Torr) following nine minutes of resting ischemia under two conditions: control (aortic and carotid baroreflex deactivation) and suction (aortic baroreflex deactivation alone). The application of neck suction to negate the CBR during cuff release caused a significant attenuation of the MSNA response and a greater decrease in mean arterial pressure; thereby signifying the importance of the CBR in the control of MSNA and maintenance of arterial blood pressure. However, when the drop in carotid sinus pressure was counteracted with neck suction a significant MSNA response was noted, indicating the dominance of the aortic baroreflex control of MSNA. Furthermore, a comparison between high-fit (HF) and average fit (AF) subjects indicated that despite an augmented baroreflex control of MSNA, HF subjects exhibited a greater decrease in mean arterial pressure compared to AF subjects. Thus, it appeared that although the arterial baroreflex appropriately increased the MSNA response to hypotension, the regulation of blood pressure remained attenuated in the HF subjects. We contend that an impaired control of vasomotion hinders blood pressure regulation in high-fit subjects.Item Effects of Endurance Training on Aortic and Carotid Baroreflex Function(1999-06-01) Smith, Scott Alan; Peter B. Raven; Michael Smith; Patricia A. GwirtzSmith, Scott Alan, Effects of Endurance Training on Aortic and Carotid Baroreflex Function. Doctor of Philosophy (Biomedical Sciences), June 1999; 122 pp; 8 tables; 10 figures; bibliography, 148 titles. Arterial bareflex control of cardiac function is dependent upon afferent input from both the aortic arch and carotid sinus bareceptors. Extensive research in animals has generated conflicting results as to the range of arterial pressures over which each baroreflex operates. Further, the complex integration of afferent signals within the medullary cardiovascular center, in reference to aortic and carotid baroreceptor input, has been characterized as additive, inhibitory, and facilitatory in nature. Such reports make it difficult to draw definitive conclusions about the behavior or central neural processing within the brainstem. In addition, these relationships have yet to be examined in humans. Therefore, the purpose of the investigations described herein, was to quantify the range of pressures over which the arterial aortic and carotid baroreflexes operate as well as to describe the interactive relationship between the aortic and carotid baroreceptors. In order to investigate these questions, we isolated the arterial, aortic, and carotid-cardiac baroreflexes in volunteer subjects generating sigmoidal stimulus-response curves for each reflex arc. Arterial and aortic baroreflex (ABR) control of heart rate (HR) was assessed by inducing graded increases and decreases in mean arterial pressure (MAP) by bolus infusion of the vasoactive agents phenylephrine (PE) and sodium nitroprusside (SN), respectively. Carotid baroreflex (CBR) function was determined utilizing ramped five second pulses of both pressure and suction applied to the carotid sinus via a neck chamber collar, independent of drug administration. The MAP at which the threshold and saturation were elicited did not differ among the reflexes examined indicating each reflex operated over a similar range of arterial pressures. Further, the simple sum of the independently driven HR response ranges of the CBR and ABR was significantly greater than that produced when both baroreceptor populations were concomitantly stimulated (i.e. arterial baroreflex) suggesting an inhibitory interaction. To investigate differential baroreflex control of HR in response to chronic endurance exercise training, a second investigation was designed implementing the reflex isolation techniques described previously. Stimulus-response relationships were compared between high fit (maximal oxygen uptake, VO2max [greater than] 60ml˖kg-1˖min-1) and average fit (VO2maxml˖kg-1˖min-1) individuals. Interestingly, neither the range of operating pressures for each reflex nor the integrative relationship between the ABR and CBR were altered as a result of aerobic training. However, the HR response range elicited from the aortic baroreceptors as a result of hypotensive and hypertensive insult was markedly attenuated in the aerobically trained population compared to their sedentary counterparts, exclusively causing a requisite reduction in arterial baroreflex sensitivity.