Abnormal cardiovascular control after spinal cord injury (SCI) results in hypotension soon after injury. Later, paroxysmal hypertension and bradycardia in response to sensory stimulation below the level of injury develop in most people with SCI. In this study, we used a radiotelemetry system, in rats (n = 7), to investigate the effect of a clinically relevant compression model of SCI at T5 spinal segment on mean arterial pressure (MAP) and heart rate (HR) at rest and in response to colorectal distension. The transducers were implanted 1 month before clip compression (50-g) injury and continuous recording of MAP and HR was established for a period of 2.5 months. SCI was associated with hypotension (86+/-3 mm Hg) at 1 day after injury. In the following 2 days, MAP gradually returned to preinjury levels. By contrast, HR increased at 1 day after SCI and remained unchanged thereafter. Three days after SCI, colorectal distension caused an increase in MAP of 8+/-2 mm Hg accompanied by bradycardia (-18 bpm). One week after SCI, colorectal distension induced an increase in MAP of 9+/-2 mm Hg and bradycardia (-41 bpm). In the following days, the magnitude of reflex hypertension gradually increased, reaching 21+/-4 mm Hg at 1.5 months after SCI. In summary, our data show that resting MAP rapidly returns to control values after SCI. Episodic hypertension associated with autonomic dysreflexia can develop in rats within 1 month after incomplete SCI.