The control of muscle sympathetic nerve activity (MSNA) via the baroreflex is an important mechanism of blood pressure control. Spontaneous sympathetic baroreflex sensitivity (BRS) is a tool used to examine how well the baroreflex buffers beat-to-beat changes in arterial pressure. Due to the lack of research around the baroreflex control of MSNA, it is unknown if an individual's sympathetic BRS reflects the end organ response and thus is indicative of how effective they are at regulating their blood pressure. It was hypothesised that poor baroreflex sensitivity was compensated for by enhanced vascular transduction, and vice versa. Given that sex differences are known to exist in regulatory mechanisms involved in cardiovascular control, these interactions were explored and contrasted in young males and females. In order to further our understanding of the regulatory mechanism of the sympathetic baroreflex, MSNA, blood pressure and superficial femoral artery (SFA) blood flow were measured to i) examine the stability and repeatability of measures of spontaneous sympathetic BRS, ii) examine whether vascular transduction, quantified on a beat-to-beat basis using two different approaches, were different between males and females, iii) examine the relationship between sympathetic BRS and vascular transduction, and iv) examine sympathetic BRS and vascular transduction during physiological stressors that drive increases in MSNA. Here I present evidence of sex differences in sympathetic baroreflex function in healthy young adults. Spontaneous sympathetic BRS was moderately stable in the same recording period and also when examined on different days. Recording periods of at least 5 min should be used when quantifying BRS as shorter durations can overestimate BRS values. Using the Fairfax method, sympathetic vascular transduction was significantly lower in males when compared with females. In contrast, the Briant method did not reveal sex differences in vascular transduction between males and females. Sympathetic BRS and vascular transduction was negatively correlated under resting conditions. This means that individuals with high sympathetic BRS have less effective vascular transduction during spontaneous changes in blood pressure. However, this was only apparent in young males; there was no relationship observed in females. Furthermore, resting MSNA did not predict sympathetic BRS or vascular transduction in either males or females. Finally, vascular transduction was significantly greater in males when quantified as the relationship between MSNA and leg vascular conductance during isometric handgrip and the cold pressor test. Sympathetic BRS was not different between males and females during the cold pressor test but was reset to a higher blood pressure range. Collectively, the studies conducted in this thesis provide insight into the dynamic nature of the baroreflex control of arterial pressure at rest, and during increases in muscle vasoconstrictor drive. Whilst this thesis provides evidence of sex differences in sympathetic BRS and vascular transduction, it also highlights the differences between the various approaches available for quantifying vascular transduction. The method chosen can have a profound effect on the findings regarding sex differences and the interaction vascular transduction has with sympathetic BRS
