The developmental origins of hypertension have been increasingly investigated in recent years. In the rat, administration of high levels of glucocorticoid during late pregnancy produces late onset hypertension in the offspring. The underlying causes of such programmed hypertension are not known, but may involve alterations in cardiovascular autonomic control. Here, we examined baroreflex and peripheral chemoreflex changes in heart rate (HR) and sympathetic nerve activity (SNA) in the rat following gestational dexamethasone administration (DEX), using the in situ working heart brainstem preparation. Pregnant dams were administered DEX (200 μg/kg s.c.) at days E15-E16. At birth, litter size was reduced to 8 and pups were left with the dam until weaning. Naïve age-matched rats were used as controls. At 3-5 weeks experiments were performed in the in situ working heart brainstem preparation (Paton, 1996). Under halothane anaesthesia, rats were transected below the diaphragm and decerebrated to the level of the superior colliculus. The rostral portion of the rat was perfused via the descending aorta using oxygenated Ringer’s solution. Perfusion pressure, HR, phrenic nerve activity (PNA) and thoracic SNA were recorded. HR and SNA responses to both baroreceptor (a ramp increase in perfusion pressure of 20-30 mmHg) and peripheral chemoreceptor stimulation (injection of 75 μL 0.03% sodium cyanide) were measured. Data are expressed as mean ± SEM and statistical significance determined using unpaired student’s t-test. There was no difference in baseline perfusion pressure (control, 65 ± 3 vs DEX, 66 ± 5 mmHg), HR (control, 327 ± 3 vs DEX, 309 ± 16 bpm) or PNA cycle length (control, 3.3 ± 0.4 vs DEX, 2.8 ± 0.3 s). Baroreflex changes in HR gain (control, -1.3 ± 0.2 vs DEX, -0.8 ± 0.2 bpm/mmHg) and SNA gain (-16 ± 4 vs -6 ± 1 % baseline/mmHg) were both lower in the DEX rat than controls (P<0.05, n=9). In contrast, the peripheral chemoreflex changes in HR (control, -161 ± 30 vs DEX, -217 ± 15 bpm) and SNA (control, 146 ± 11 vs DEX, 185 ± 10 % baseline, P<0.05, n=5) were augmented, although there was no difference in the change in PNA cycle length (decrease: control, 2.0 ± 0.4 vs DEX, 1.7 ± 0.2 s). The results indicate that cardiovascular autonomic reflexes are altered in the DEX model of programmed hypertension in such a way as to facilitate an increase in sympathetic drive. This may contribute to the ontogeny of hypertension in this model.