Stimulation by bradykinin of afferent vagal C-fibers with chemosensitive endings in the heart and aorta of the dog.

Abstract

Bradykinin applied directly to the epicardium evokes a reflex increase in blood pressure by stimulating sympathetic afferent nerve endings in the heart; injected into the coronary artery, it evokes vagally mediated reflex decreases in heart rate and blood pressure. The afferents initiating these latter depressor effects have not been identified. Vagal sensory nerve endings in the heart which are stimulated by bradykinin were determined. In anesthetized dogs impulses from afferent vagal fibers with endings in the heart and aorta were recorded and bradykinin (0.3-1.0 .mu.g/kg) was injected into the left atrium. Neither A- nor C-fiber mechanoreceptors nor aortic body chemoreceptors were stimulated directly by bradykinin; any changes in firing of atrial or ventricular mechanoreceptors or of aortic baroreceptors or chemoreceptors were secondary to the cardiovascular effects of bradykinin. Of 20 irregularly discharging vagal C-fibers with chemosensitive endings in the left ventricle, left atrium and aorta 16 were stimulated by bradykinin; firing increased from 0.2 .+-. 0.1 to 7.8 .+-. 1.4 (mean .+-. SE) impulses/s and usually remained above control for .apprxeq. 30 s. These chemosensitive endings were not stimulated by ventilating the lungs with 5% O2 in N2, but they were stimulated by injecting capsaicin or phenyl diguanide into the left atrium. Four chemosensitive endings in the ventricular epicardium were stimulated by dripping bradykinin (1 .mu.g/ml) onto the heart. These chemosensitive vagal C-fibers apparently are responsible for the reflex decreases in heart rate and blood pressure elicited by bradykinin.