Bradykinin applied directly to the epicardium evokes a reflex increase in blood pressure by stimulating sympathetic afferent nerve endings in the heart, but 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. We have attempted to determine which vagal sensory nerve endings in the heart are stimulated by bradykinin. In anesthetized dogs, we recorded impulses from afferent vagel fibers with endings in the heart and aorta and injected bradykinin (0.3-1.0) μg/kg) 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, being secondary to the cardiovascular effects of bradykinin. However, 16 of 20 irregularly discharging vagal C-fibers with chemosensitive endings in the left ventricle, left atrium, and aorta were stimulated by bradykinin; firing increased from 0.2 ± 0.1 to 7.8 ± 1.4 (mean ± SE) impulses/sec and usually remained above control for about 30 seconds. These chemosensitive endings were not stimulated by ventilating the lungs with 5% O 2 in N 2, but they were stimulated by injecting capsaicin or phenyl diguanide into the left atrium. Four chemosensitive endings in the ventricular epicardium were also stimulated by dripping bradykinin (1 μg/ml) onto the heart. We suggest that these chemosensitive vagal C-fibers are responsible for the reflex decreases in heart rate and blood pressure elicited by bradykinin.
|Original language||English (US)|
|Number of pages||9|
|State||Published - 1980|
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine