Description

African American (AA) adults have a greater prevalence of developing cardiovascular and renal disease (CVRD) than White (W) adults. Elevated sympathetic nervous system activity 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 outflow to the kidneys in AA adults might be exaggerated, 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 study 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. In Specific Aim 1, the investigators will test the hypothesis that the renal vasoconstrictor response to acute dynamic exercise is exaggerated in healthy young AA compared to W adults. Specifically, the investigators will measure RBF and blood pressure at rest and during cycling exercise to calculate renal vascular resistance responses to exercise, enabling us to 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 Specific Aim 2, the investigators will test the hypothesis that the renal vasoconstrictor response to non-exercise sympathetic stressors is exaggerated in healthy young AA compared to W adults. Specifically, the investigators will measure RBF and blood pressure at rest and during a cold pressor and mental stress tests to calculate renal vascular resistance responses to these non-exercise sympathetic stressors, enabling us 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.

Using the highly innovative approach of Doppler ultrasound to measure RBF during exercise and non-exercise sympathetic stressors non-invasively and with high temporal resolution will enable us to assess the renal vasoconstrictor response to sympathetic stressors in healthy AA adults prior to development of CVRD, so the underlying integrative physiological responses to sympathetic activation in AA adults can be understood. Findings from this study in this understudied yet clinically significant area will contribute to the ultimate goal of creating and implementing treatment strategies to reduce the risk of developing CVRD in AA adults.