The renin angiotensin system has been implicated in the etiology of the cardiovascular complications of diabetes. Our studies extend these findings to show a specific role for angiotensin AT1a receptors in mediating diabetes-induced hypertension. Male angiotensin AT1a knockout (Ang AT1aKO) and wild type (AT1aWT) mice with arterial telemetric catheters were injected with streptozotocin (STZ, 150 mg/kg, ip). The STZ dose was selected on the basis of a dose response experiment in C57/Bl mice. Blood glucose, water intake, body weight, blood pressure (BP) and heart rate (HR) were measured over a two week period. Estimates of BP and HR variance (BPV and HRV) and their low and high frequency domains were also determined. STZ induced similar levels of hyperglycemia and polydypsia in the groups. Mean arterial pressure (MAP) was increased from 100±6 to124±6 mmHg in diabetic AT1aWT. MAP was unchanged in AT1aKO (80±4 vs. 85±5 mmHg, basal vs. STZ). Treatment with an ACE inhibitor, captopril, produced a greater reduction in MAP (-18%) in diabetic AT1aWT than in AT1aKO (- 3.4%). BPV was lower in AT1aKO (19±0.5 vs. 9±2 mmHg², AT1aWT vs. AT1aKO). Diabetes reduced BPV, but only in AT1aWT (19±0.5 vs. 8±1 mmHg², basal vs. STZ). There were no changes in HR in either group. In AT1aKO, STZ increased HRV and its high frequency domain with no changes seen in AT1aWT. Results document that Ang AT1a receptors are critical in diabetes-induced hypertension and in cardiac autonomic responses.