Relative burst amplitude of muscle sympathetic nerve activity (MSNA) is an indicator of augmented sympathetic outflow and contributes to greater vasoconstrictor responses. Evidence suggests anxiety-induced augmentation of relative MSNA burst amplitude in patients with panic disorder, thus we hypothesized that acute stress would result in augmented relative MSNA burst amplitude and vasoconstriction in individuals with chronic anxiety. Eighteen participants with chronic anxiety (ANX, 8 men/10 women, 32{plus minus}2 years) and 18 healthy controls with low/no anxiety (CON, 8 men/10 women, 39{plus minus}3 years) were studied. Baseline MSNA and 24-hour blood pressure were similar between ANX and CON (P>0.05); however, nocturnal systolic blood pressure % dipping was blunted among ANX (P=0.02). Relative MSNA burst amplitude was significantly greater among ANX compared with CON immediately preceding (anticipation) and during physiological stress (2-min cold pressor test, ANX: 73{plus minus}5% vs. CON: 59{plus minus}3% AU, P=0.03) and mental stress (4-min mental arithmetic, ANX: 65{plus minus}3% vs. CON: 54{plus minus}3% AU, P=0.02). Increases in MSNA burst frequency, incidence, and total activity in response to stress were not augmented among ANX compared with CON (P>0.05), and reduction in brachial artery conductance during cold stress was similar between ANX and CON (P=0.92). Relative MSNA burst amplitude during mental stress was strongly correlated with state (P<0.01) and trait anxiety (P=0.01) (State-Trait Anxiety Inventory), independent of age, sex and BMI. Thus, in response to acute stress, both mental and physiological, individuals with chronic anxiety demonstrate selective augmentation in relative MSNA burst amplitude, indicating enhanced sympathetic drive in a population with higher risk for cardiovascular disease.