Search for a cardiac nociceptor: stimulation by bradykinin of sympathetic afferent nerve endings in the heart of the cat.

Abstract

The effect of bradykinin on impulse traffic was examined in sympathetic afferent fibers from the heart, great vessels and pleura to identify cardiac nociceptors that (on the basis of their functional characteristics) may initiate cardiac pain. Afferent endings excited by bradykinin were of 2 types. Those located in the heart, great vessels or overlying pleura had a cardiac rhythm of discharge and were stimulated by an increase in blood pressure or cardiac volume. Bradykinin increased mechanoreceptor firing; some endings appeared to be stimulated directly by bradykinin (chemosensitive); others were sensitized so that they responded more vigorously to the pulsatile mechanical stimulation associated with the cardiac cycle (mechanosensitive). Others rarely fired with a cardiac rhythm, and even large increases in aortic or left ventricular pressure had little effect on impulse frequency. Tachyphylaxis occurred when the interval between successive applications of bradykinin was 20 min or less. Because of their responsiveness to changes in pressure and their sensitivity to light touch, the mechanosensitive endings appear unlikely to subserve a primarily nociceptive function, although they may be responsible for evoking some of the components of the pseudoaffective response. The chemosensitive endings apparently act as cardiac nociceptors.