Hypothesis: Sympathoexcitation and sodium retention contribute to age-related hypertension (HTN). Methods: Three, 8, and 16 month old male SD rats underwent an IV volume expansion (VE; 5% BW) and MAP, HR, urine output and paraventricular nucleus (PVN) neuronal activation (c-Fos expression) were assessed. In separate groups of rats fed a 21 day normal (NS; 0.6% NaCl) or high salt (HS; 4% NaCl) diet, measures of 1) ex vivo afferent renal nerve (ARN) activity (norepinephrine (NE)-evoked substance P release) or 2) MAP, HR, NCC activity (ΔUNaV to IV HCTZ, 2mg/kg) and sympathetic tone (plasma and renal NE content, ΔMAP to IV hexamethonium) were assessed. Separate groups of rats underwent bilateral renal denervation (RDNX) or chronic NCC antagonism (SC HCTZ, 4mg/kg/d, 14d) and MAP was assessed (N=4/gp). Results: Acute VE-evoked natriuresis, diuresis, and PVN parvocellular neuronal activation were impaired in aged rats. Aged rats exhibited reduced ARN activity on a NS diet and failed to increase ARN activity during a HS diet. In aged rats, basal MAP, NCC activity and sympathetic tone were increased and HS-evoked suppression of NCC activity and sympathetic tone was impaired. Chronic NCC antagonism and RDNX attenuated age-related HTN (MAP [mmHg] 16mo 149±3 vs RDNX 139±1 vs SC HCTZ 136±5, P<0.05). Conclusion: Our data suggest that the ARN, which have been implicated in the regulation of sympathetic outflow and renal sodium excretion, are impaired in age-related HTN. We speculate that an age-related decrease in ARN activity promotes sympathoexcitation, perhaps in part via reduced activation of PVN sympathoinhibitory parvocellular neurons, resulting in NCC-mediated sodium retention and HTN.