Voluntary Exercise Prevents Hypertensive Response Sensitization (HTRS)

Abstract

Exercise training has profound effects on the renin‐angiotensin system (RAS), inflammatory mediators and ROS production, all of which influence autonomic nervous system activity and regulates cardiovascular function in both physiological and pathophysiological states. Our previous studies using an Induction‐Delay‐Expression (IND‐DEL‐EXP) paradigm to study HTRS demonstrated that various challenges (stressors) including a subpressor dose of angiotensin (ANG) II given during IND, resulted in HTRS to a subsequent treatment with slow‐pressor dose of ANG II during EXP. The present study tested whether voluntary exercise would protect against subpressor ANG II‐induced HTRS in rats. Adult male rats were given access to either “blocked” (sedentary rats) or functional running (exercised rats) wheels for 10 weeks, and the IND‐DEL‐EXP paradigm was applied for the rats during the last 4 weeks. A subpressor dose of ANG II (10 ng/kg/min) given during IND produced an enhanced hypertensive response to a pressor dose of ANG II (120 ng/kg/min) given during EXP in sedentary rats in comparison to sedentary animals that received saline (vehicle control) during IND. Voluntary exercise did not attenuate the pressor dose of ANG II‐induced hypertension, but prevented the induction of HTRS seen in sedentary animals. Moreover, the subpressor dose of ANG II given during IND induced upregulation of mRNA expression of several RAS pro‐hypertensive components and proinflammatory cytokines in the lamina terminalis (LT), which was attenuated by exercise. Also, RAS antihypertensive components, such as angiotensin type 2 receptor (AT2‐R) and Mas‐R, were upregulated by subpressor dose of ANG II in exercised rats. These results indicate that exercise training plays a beneficial role in preventing HTRS and that this is associated with reduced expression of increased pro‐hypertensive components of the RAS and of inflammatory mediators and by enhanced expression of RAS antihypertensive components in the CNS.Support or Funding InformationThis work is supported by the NIH grants HL‐14388 (AKJ), HL‐98207 (AKJ & BX), HL‐139575 (AKJ & BX).This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.