Afferent neurons contained within cardiac sympathetic nerves can have excitatory influences on central sympathetic outflow. The normal or pathological circumstances during which such excitatory reflexes occur are not well understood. The purpose of this research was to investigate the possibility that cardiac sympathetic afferent neurons make a significant contribution to cardiovascular control during myocardial ischemia. Afferent influences on renal nerve activity were characterized during occlusion of coronary arteries and in response to chemical stimulation of cardiac receptors by bradykinin. Reflexes were investigated in chloralose-anesthetized cats in which arterial baroreceptors had been denervated. In vagotomized cats afferent stimulation by coronary occlusion or by bradykinin caused significant increases in renal nerve activity. When vagi remained intact, coronary occlusion or epicardially applied bradykinin caused increases, decreases biphasic responses or no significant change in renal nerve activity. Thus, excitatory reflexes could be initiated by the sympathetic afferent neurons in some cats despite simultaneous vagal afferent stimulation. The responses to chemical stimulation followed the same pattern as those to coronary occlusion suggesting that a component of the afferent stimulus during ischemia may be chemical in nature. Finally, the central pathways mediating these excitatory reflexes were investigated by comparing responses to epicardially applied bradykinin in vagotomized cats prior to and following high cervical spinal cord transection or midcollicular decerebration. Excitation of renal nerve activity by this chemical afferent stimulation was reduced but still present in spinalized cats and unchanged in decerebrate cats. Thus spinal pathways may mediate at least a component of these excitatory reflexes but forebrain regions are not essential to their initiation. In summary, these findings are consistent with the contentions that: (1) cardiac sympathetic afferent neurons may initiate significant excitatory reflexes during myocardial ischemia; (2) such reflexes may be due, in part, to chemical stimulation of cardiac receptors; and (3) these reflexes can be mediated partially by spinal pathways.