In anesthetized and artificially ventilated cats, we recorded the impulse activity of 23 afferent sympathetic unmyelinated fibers with left ventricular endings, dissected from the left sympathetic rami T3 and T4. All fibers displayed a spontaneous discharge at a rate of 0.79 ± 0.2 (mean ± SE) impulses/sec. During constriction of the thoracic aorta, the discharge increased to 1.92 ± 0.2 impulses/ sec. During myocardial ischemia, produced by interruption of left main coronary artery perfusion, supplied through an extracorporeal pump, the impulse activity increased to 1.73 ± 0.3 impulses/sec. The mean latency for this excitation was 16.5 ± 1.5 sec. The intracoronary administration of bradykinin (5 and 10 ng/kg) elicited a marked increase in impulse activity that, following 5 ng/kg, reached 2.06 ± 0.2 impulses/sec, after a latency of 18 ± 2 sec and in absence of significant hemodynamic changes. Myocardial ischemia and bradykinin never revealed the existence of silent afferent fibers included in the split nerve strand. The results obtained with this experimental model indicate that the ventricular endings of these afferent sympathetic unmyelinated fibers act as "polymodal" receptors. We hypothesize that the peripheral mechanism for cardiac nociception involves intensive excitation of fibers discharging spontaneously and not recruitment of silent fibers which are purely nociceptive in function. Circ Res 48: 69-75, 1981