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Myocardial ischemia stimulates cardiac spinal afferents to initiate a sympathoexcitatory reflex. However, the pathways responsible for generation of increased sympathetic outflow in this reflex are not fully known. In this study, we determined the role of the paraventricular nucleus (PVN) in the cardiogenic sympathetic reflex. Renal sympathetic nerve activity (RSNA) and blood pressure were recorded in anesthetized rats during epicardial application of 10 µg/ml bradykinin. Bilateral microinjection of muscimol (0.5 nmol), a GABAA receptor agonist, was performed to inhibit the PVN. In 10 vehicle-injected rats, epicardial bradykinin significantly increased RSNA 178.4 ± 48.5 % from baseline and mean arterial pressure from 76.9 ± 2.0 to 102.3 ± 3.3 mmHg. Microinjection of muscimol into the PVN significantly reduced the basal blood pressure and RSNA (n = 12). Following muscimol injection, the bradykinin-induced increases in RSNA (111.6 ± 35.9% from baseline) and mean arterial pressure (61.2 ± 1.3 to 74.5 ± 2.7 mmHg) were significantly reduced compared to control responses. The response remained attenuated even when the basal blood pressure was restored to the control. In a separate group of rats (n = 9), bilateral microinjection of the ionotropic glutamate antagonist kynurenic acid (4.82 or 48.2 nmol in 50 nl