Clinically, it has been observed that stroke causes a number of cardiovascular disturbances that are detrimental to prognosis and may cause death. We have developed an experimental model of stroke, a middle cerebral artery occlusion in the rat, that can mimic the acute cardiovascular responses observed clinically. This model has clearly demonstrated that the insular cortex is necessary to produced the autonomic changes and that these changes are exacerbated by right-sided infarcts and increasing age. In addition, we have demonstrated that there are neurochemical changes associated with our stroke model that may mediate the cardiovascular complications. In particular, an increase in dynorphin in the central nucleus of the amygdala occurs with a peak at 3 to 5 days after the stroke and is directly due to damage in the insular cortex. Finally, we have shown that there is a similar time course in the exaggerated cardiovascular responses to stress following middle cerebral artery occlusion. Direct injection of dynorphin into the central nucleus of the amygdala can enhance the cardiovascular response obtained by stimulation of the acoustic stress pathway. These observations have direct relevance to clinical stroke.