On the early onset of vascular stiffening and sexual dimorphism of sympathetic control in the spontaneously hypertensive rat

The purpose of this thesis was to explore the role of the sympathetic nervous system (SNS) in hindlimb vasomotor control during the development of hypertension (HT). Using an animal model of essential HT (the spontaneously hypertensive rat [SHR]) we demonstrated that neuropeptide Y (NPY) and the Y1 receptor (Y1R) play a greater role in modulating hindlimb hemodynamics in the early stages of HT compared to normotensive controls (Wistar Kyoto [WKY]). Hindlimb vascular mechanics (compliance [C] and viscoelasticity [K]) were assessed using a modified Windkessel model developed in our laboratory. The hindlimb mechanics did not appear to be regulated by NPY or the Y1R specifically, but the SNS did appear to regulate the hindlimb mechanics in both SHRs and WKY animals. The use of female animals in physiologic research is limited, thus the role of the SNS in developing HT in females is unknown. Finally, differences in the hemodynamic and hindlimb vascular mechanics between male and female animals were examined. Female animals exhibited augmented MAP and HR relative to males in conjunction with greater stiffness and viscoelasticity in both SHR and WKY animals. Female SHRs also appeared to lose SNS control over the stiffness and viscoelastic properties of the hindlimb vascular bed, while male SHRs maintained this control. These sexually dimorphic characteristics provide evidence for a novel proposed mechanism of cardiovascular regulation in young female rats