“…1 Besides Jarisch and Zotterman, 2 who confirmed these results, a host of other investigators contributed greatly to increase our knowledge about the coronary BJR, involving receptors, couched in different terminologies, as ventricular mechanosensitive or chemosensitive neuroreceptors, mostly located in the inferioposterior left ventricular wall, which discharge irregularly and sporadically into small nonmyelinated afferent C-fibers in the vagi. [2][3][4][5] Although these receptors have not been described anatomically or histologically, and the precise mechanisms and the natural stimulus to the cardioinhibitory reflex response are insufficiently understood, stimulation by stretch, distension of an infarcted area, or chemical substances are thought to modulate the arterial baroreflex mediating efferent vagal activation. 17 Fundamental experimental evidence suggests that locally released mediators that occur within minutes after the onset of ischemia, and particularly during reperfusion, such as prostaglandins, serotonin, and oxygenderived free radicals, may activate the cardiac vagal afferent pathways.…”