Reflex coronary vasodilation evoked by chemical stimulation of cardiac afferent vagal C fibres in dogs.

1. Veratridine injected into the coronary circulation stimulates afferent vagal endings in the heart to evoke bradycardia and systemic hypotension (Bezold-Jarisch reflex, coronary chemoreflex) and coronary vasodilation. We have examined certain features of the reflex coronary vasodilator response in anaesthetized dogs. 2. When the circumflex coronary artery was perfused at constant pressure (100 mmHg), injection of veratridine (0.3 micrograms kg-1) into the anterior descending artery decreased blood pressure and heart rate, and increased circumflex blood flow by 54%; when heart rate was kept constant, circumflex flow increased by 57%. The increase in circumflex flow was reduced 63% by atropine, and finally abolished by phentolamine. 3. During severe coronary underperfusion (perfusion pressure 45 mmHg), veratridine still increased coronary flow by 35%, an increase amounting to 24-64% of the coronary vascular reserve. Flow increased in all layers of the myocardium, but the relative distribution of flow between subendocardial and subepicardial layers was unaltered. 4. Veratridine stimulates both mechanosensitive and chemosensitive cardiac endings. Stimulating chemosensitive afferents selectively by injecting capsaicin (1.5 micrograms kg-1) into the anterior descending artery decreased blood pressure and heart rate, and increased circumflex flow by 50% (and by 36% when heart rate was kept constant). 5. In ten of fifteen dogs, veratridine and capsaicin still evoked coronary vasodilatation when vagal A fibres were blocked selectively by cooling to 7.5 degrees C, the increase in coronary flow averaging 45% of that at 37 degrees C. All responses were abolished by cooling to 0 degrees C. 6. We conclude that coronary vasodilatation can be evoked by selective stimulation of cardiac chemosensitive vagal C fibres, although the coronary vasodilation of the veratridine-induced Bezold-Jarisch reflex may be due to stimulation of both mechanosensitive and chemosensitive C fibres. We speculate that during periods of coronary underperfusion ischaemic stimulation of chemosensitive vagal C fibres evokes a reflex dilatation of the coronary vascular bed that supplements the dilatation dependent upon autoregulatory mechanisms.