Epileptic seizures are often accompanied by increased sympathetic cardiovascular activity (even interictally), but it remains unknown whether this increased activity is of central and/or peripheral origin. Hence, this study investigated the cardiovascular alterations produced by amygdala kindling in awake and pithed Wistar rats. Blood pressure (BP) and heart rate (HR) were initially recorded by tail cuff plethysmography in awake control, sham-operated and amygdala-kindled rats before and 24 hr after the kindling process. The after-discharge threshold (ADT) was measured under different conditions to correlate brain excitability with BP and HR in kindled rats. Twenty-four hours after the last kindling seizure, (i) HR, systolic and diastolic BP were increased and (ii) only higher HR values correlated with lower ADT values. Forty-eight hr after the last kindled seizure, all rats were pithed and prepared for analysing the tachycardic, vasopressor and vasodepressor responses by (i) stimulation of the sympathetic or sensory vasodepressor CGRPergic out-flows (stimulus-response curves, S-R curves) and (ii) intravenous injections of noradrenaline or a-CGRP (dose-response curves, D-R curves). Interestingly, (i) the tachycardic S-R and D-R curves were attenuated, whilst the CGRPergic S-R and D-R curves were potentiated in kindled rats, and (ii) the vasopressor noradrenergic S-R and D-R curves were not significantly different in all groups. Therefore, the kindling process may be associated with overstimulation in the central sympathetic and sensory out-flows interictally, producing (i) peripheral attenuation of cardiac sympathetic out-flow and b-adrenoceptor activity and (ii) peripheral potentiation of vasodepressor sensory CGRPergic out-flow and CGRP receptor activity.Epilepsy is a disorder characterized by a pre-disposition to generate spontaneous and recurrent seizures [1]. Postictal (period after a seizure characterized by a reduced susceptibility to present subsequent seizures) and interictal (period between seizures characterized by a susceptibility to present subsequent seizures) phenomena reflect changes in the brain induced by epilepsy such as depression, aggressive behaviour and autonomic dysfunction [2]. In this regard, seizures induce severe autonomic changes such as hyperventilation, apnoea and changes in blood pressure (BP) and heart rate (HR) [3,4] (even interictally). Moreover, several lines of evidence have shown (i) interictal cardiac autonomic dysfunction in patients with temporal lobe epilepsy, such as impaired HR responses and diminished HR variability [5,6], and (ii) higher basal HR in patients with complex partial and secondarily generalized seizures than in control or other epileptic patients [7].Further studies in animal models have also demonstrated a possible autonomic dysfunction associated with epilepsy. For example, Pansani et al. [8] have observed in amygdala-kindled rats (i) a correlation between the number of seizures induced by electrical amygdala kindling and ictal tachycardia, wh...