Neurovascular Control of Renal Blood Flow During Exercise in African American Adults

项目总结

Project Summary African American (AA) adults have a greater risk for developing cardiovascular and renal disease (CVRD) than White (W) adults. Elevated sympathetic nervous system activity, usually occurring in response to stressors, is associated with increased incidence of CVRD. Physical exertion, such as exercise, acutely increases sympathetic nervous system activity directed towards the kidneys, resulting in renal vasoconstriction and reduced renal blood flow (RBF). Limited research shows that healthy young AA adults exhibit exaggerated sympathetic responsiveness both at rest and during sympathetic activation, which may be a major contributor to the increased risk of CVRD in this population. However, the acute renal vasoconstrictor response to any sympathetic nervous system activation has not been investigated to date in AA adults. During sympathetic nervous system activation such as exercise, sympathetic neural activity directed to the kidneys and/or the resultant vascular response might be exaggerated in AA adults, contributing to greater renal vasoconstriction and a larger reduction in RBF. Over time, this exaggerated neurovascular response to sympathetic activation could have a negative cumulative effect on the kidneys, which could be a contributing factor to the greater incidence of CVRD in this population. Therefore, this proposal aims to examine the renal vasoconstrictor response to sympathetic stressors in healthy AA adults prior to development of CVRD, which will be achieved via two specific aims. Our first aim is to determine the renal vasoconstrictor response to acute dynamic exercise in healthy young AA adults compared to healthy young W adults. Specifically, we will use state-of-the-art methods to measure RBF velocity and BP at rest and during acute cycling exercise to calculate renal vascular resistance responses to exercise. We will test the hypothesis that healthy young AA adults exhibit an exaggerated renal vasoconstrictor response to acute cycling exercise compared to healthy young W adults. In our second aim, we will assess the renal vasoconstrictor response to non-exercise sympathetic stressors in healthy young AA adults compared to healthy young W adults. Specifically, we will measure RBF velocity and BP at rest and during cold pressor and mental stress tests to calculate renal vascular resistance responses to these non-exercise stressors to test the hypothesis that healthy young AA adults exhibit exaggerated renal vasoconstrictor responses to non-exercise sympathetic stressors compared to healthy young W adults. We will use the highly innovative approach of Doppler ultrasound to measure RBF during exercise and non-exercise sympathetic stressors non-invasively and with high temporal resolution to complete these specific aims. This novel approach by our experienced research team to assess the renal vasoconstrictor response to sympathetic stressors in AA adults will provide new, mechanistic insights in this understudied yet clinically significant area. The findings from this project will advance our understanding of why AA adults have elevated CVRD risk, with implications for future efforts toward prevention of CVRD.