Hypertension (HTN) among young adults is a common condition that increases cardiovascular risk and causes end organ damage early in its onset. Muscle sympathetic nerve activity (MSNA) is elevated in young patients with HTN. A potential source of sympathetic activation are the peripheral chemoreceptors; particularly the carotid body. Animal studies indicate that the organ may play a critical role in the onset of hypertension (1). Human studies have been fewer and the results equivocal (2) (3). The aim of this study was to identify whether young adults with primary HTN exhibit elevated carotid body activity as measured by their ventilatory response to hypoxia (HVR) at rest and during exercise. 10 untreated, stage 1 HTN (3 female, mean ± standard deviation (SD) age; 26 ± 4 years) were recruited from a specialist HTN clinic. 10 normotensive (NTN) controls (5 female, age; 28 ± 2 years) were recruited from the local area. HTN was confirmed using a validated 24-hour ambulatory blood pressure monitor. Each participant underwent a maximal cardiopulmonary exercise test on an upright cycle ergometer to assess peak oxygen consumption (VO2 peak). HVR was assessed using the transient method (4). Briefly, participants were exposed to short periods of hypoxia by delivery of between 1-10 breaths of 100% nitrogen titrated into the inspiratory circuit using an electronic switching valve. This was repeated 4 to 5 times to provide a range of hypoxic exposures. Assessment of HVR was repeated in the presence of an intravenous dopamine infusion (2mcg/kg/min) to block carotid body afferent activity and a saline infusion as a control (4). HVR was next assessed during low intensity (30-40% VO2 peak) exercise during saline and dopamine infusions. HVR was calculated by plotting minute ventilation against SpO2%. The gradient of the linear regression line was used for HVR as measured in L/min/%SpO2. A 2-way ANOVA was used to compare HVR during both infusions at rest and exercise. An independent samples t-test was used for non-repeated measures. There was no difference in VO2 Peak between the two groups (NTN: 38 ± 5.3 mL/Kg/min, HTN: 32.2 ± 7.7 mL/Kg/min, P=0.07). There was no difference in HVR during saline infusion between groups at rest (NTN: -0.219 ± 0.069 L/min/%SpO2, HTN: -0.275 ± 0.077 L/min/%SpO2, P=0.59). HVR rose significantly during exercise in both groups (NTN: -0.702 ± 0.21 L/min/%SpO2, N=8, HTN: -0.665 ± 0.23 L/min/%SpO2, n=10, P=0.009), but there was no difference between groups (P=0.95). Infusion of dopamine caused a significant reduction in HVR in both groups (P=0.0006) demonstrating that HVR is largely attributable to the carotid body. In conclusion, there is no difference in HVR as mediated by the carotid body between normotensive and hypertensive young adults at rest or during submaximal exercise.