High gestational levels of glucocorticoid are linked to increased incidence of cardiovascular (especially hypertension) and behavioural disorders in later life (1). Generally, such programmed hypertension has been attributed to changes in renal and vascular function, while behavioural disorders have been associated with changes in the hypothalamic pituitary axis, as well as other areas of the central nervous system. In view of these changes in the central nervous system following high prenatal glucocorticoid, and the recent interest in the role of the autonomic nervous system in the aetiology of hypertension (2), we hypothesize that prenatal glucocorticoid programming of hypertension may also involve alterations in autonomic function. In this study, we exposed pregnant dams to steroid and in her offspring examined spontaneous baroreflex gain (sBRG), pulse interval variability (PIV) and systolic blood pressure variability using radiotelemetry. Values expressed are mean ± SEM and statistical analyses were performed using a two-tailed Student’s t test. At E15-E16, pregnant Sprague Dawley dams were administered with the synthetic glucocorticoid dexamethasone (DEX; 200 μg kg^-1 s.c.). An equal volume of saline was administered to the control dams. The offspring (3-5 weeks) were anesthetised with ketamine (60 mg kg^-1) and medetomidine (250 μg kg^-1) and implanted with a blood pressure (BP) radiotelemetry transmitter. After 1 week recovery, 24 h pulsatile BP was recorded in the unanaesthetized, freely moving rat, and sBRG, PIV and BPV were calculated. At week 5 postnatal, BP was not different in the offspring of DEX-treated dams than controls (DEX, 118.7±2.9 vs control, 122.5±2.0 mmHg, P=0.2); however, sBRG (DEX, 0.36±0.03 vs control, 0.54±0.04 ms mmHg^-1, P<0.01), the very low frequency (3.33±0.44 vs 4.76±0.57 ms², P<0.05) and low:high frequency (0.19±0.03 vs 0.26±0.02, P<0.05) components of PIV were reduced. At week 9, BP was approximately 10 mmHg higher in DEX-treated offspring than controls (130.6±3.1 v 140.8±4.0 mmHg, P<0.05). sBRG (0.34±0.02 v 0.49±0.05, P<0.05), very low frequency (3.88±0.56 v 5.31±0.47, P<0.05) and low:high frequency (0.16±0.01 v 0.25±0.02, P<0.01) components of PIV remained reduced, while the high frequency component of PIV was increased (11.93±1.04 v 9.43±0.45, P<0.05). Our results show that following prenatal administration of DEX in the rat, cardiovascular autonomic function is already disturbed at week 5 postnatal, before the onset of hypertension,. Alterations in cardiovascular autonomic function may therefore contribute to programmed hypertension in this model.