Harald M. Stauss, M.D., Dept of Health and Human Physiology, The University of Iowa. Friday, September 23, 2016, 11:00-12:00, LIB-110. Synopsis: While the role of elevated sympathetic nervous system activity for hypertension-induced cardiovascular end-organ damage is widely accepted, the role of the parasympathetic nervous system in hypertension has been less thoroughly investigated. Parasympathetic activity is often reduced in hypertension and reduced parasympathetic tone has been associated with greater cardiovascular mortality. Furthermore, the parasympathetic nervous system can activate anti-inflammatory pathways. Thus, we hypothesized that restoring parasympathetic nervous system activity by chronic vagal nerve stimulation (VNS) may alleviate cardiovascular end-organ damage in stroke-prone spontaneously hypertensive rats (SHR-SP) on high-salt diet. Four weeks of chronic VNS prevented the progression of endothelial dysfunction and aortic stiffening observed in sham stimulated SHR-SP on high-salt diet. Correlations of pro- and anti-inflammatory cytokines measured in spleen extracts and serum with vascular parameters suggest that VNS elicits its beneficial vascular effects through an anti-inflammatory action.