Spinal reflexes dominate cardiovascular control after spinal cord injury (SCI). These reflexes are no longer restrained by descending control and they can be impacted by degenerative and plastic changes within the injured cord. Autonomic dysreflexia is a condition of episodic hypertension that stems from spinal reflexes initiated by sensory input entering the spinal cord caudal to the site of injury. This hypertension greatly detracts from the quality of life for people with cord injury and can be life-threatening. Changes in the spinal cord contribute substantially to the development of this condition. Rodent models are ideal for investigating these changes. Within the spinal cord, injury-induced plasticity leads to nerve growth factor (NGF)-dependent enlargement of the central arbor of a sub-population of sensory neurons. This enlarged arbor can provide increased afferent input to the spinal reflex, intensifying autonomic dysreflexia. Treatments such as antibodies against NGF can limit this afferent sprouting, and diminish the magnitude of dysreflexia. To assess treatments, a compression model of SCI that leads to progressive secondary damage, and also to some white matter sparing, is very useful. The types of spinal reflexes that likely mediate autonomic dysreflexia are highly susceptible to inhibitory influences of bulbospinal pathways traversing the white matter. Compression models of cord injury reveal that treatments that spare white matter axons also markedly reduce autonomic dysreflexia. One such treatment is an antibody to the integrin CD11d expressed by inflammatory leukocytes that enter the cord acutely after injury and cause significant secondary damage. This antibody blocks integrin-mediated leukocyte entry, resulting in greatly reduced white-matter damage and decreased autonomic dysreflexia after cord injury. Understanding the mechanisms for autonomic dysreflexia will provide us with strategies for treatments that, if given early after cord injury, can prevent this serious disorder from developing.