Reflex circulatory changes mediated by capsaicin sensitive cardiac afferent neurones were studied in anaesthetised, open chest dogs. Application of capsaicin to the epicardium of the left ventricle, either in single doses (0.01-100 micrograms) or by superfusion (20 micrograms X min-1), consistently resulted in dose related increases in blood pressure and heart rate. These responses were not affected by bilateral vagotomy but were abolished or reversed by bilateral sectioning of the upper thoracic (T1-T4) white rami communicantes and stellectomy. Injection of capsaicin (0.3-1 microgram X kg-1) into the left circumflex coronary artery caused either systemic hypotension and bradycardia (70.3% of experiments), a pressor response associated with tachycardia (13.5%), or a biphasic effect with an initial rise and then fall in blood pressure and heart rate (16.2%). With intravenous injections of capsaicin (3-5 micrograms X kg-1) the response was invariably cardioinhibitory and depressor. The reflex bradycardia and hypotension evoked with either intracoronary or intravenous injections of capsaicin were reversed after bilateral vagotomy to increases in cardiac rate and blood pressure. The post-vagotomy tachycardia occurring with intracoronary capsaicin could be abolished by beta adrenoceptor blockade with propranolol (0.5 mg X kg-1 iv), whereas ganglionic transmission blockade with pentolinium (0.5 mg X kg-1 iv) eliminated both the tachycardia and pressor effects. The results indicate that in the dog's heart capsaicin sensitive afferent neurones capable of affecting the circulatory system have both vagal and spinal sympathetic origin. It is suggested that capsaicin induced excitatory cardiogenic reflex is nociceptive in nature and may involve activation of substance P containing afferent fibres incorporated in cardiac sympathetic nerves.

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Experiments were performed on anaesthetized, open-chest dogs to determine the reflex effects on systemic blood pressure and heart rate produced by stimulation of the parietal pericardium with bradykinin and nicotine, and to compare these effects with those evoked by application of these substances to the visceral pericardium (epicardium) of the left ventricle. Bradykinin (0.01-6.0 micrograms) elicited reflex increases in blood pressure and heart rate when applied either to the parietal pericardium or to the ventricular epicardium; the responses evoked from both sites were dose-dependent from the threshold of 0.01 micrograms to a maximum at 1.0 micrograms of bradykinin. The reflex effects of bradykinin were not affected by either vagotomy or phrenic nerve section, but were suppressed by bilateral sectioning of the upper thoracic (T1-T4) white rami communicantes and stellectomy. In contrast to bradykinin, nicotine (20-100 micrograms) failed to produce any change in blood pressure and heart rate when applied to the parietal pericardium and evoked depressor responses when applied to the epicardium of the left ventricle; these depressor effects of nicotine were abolished by vagotomy. The results indicate that sympathetic, but not vagal, afferent endings innervating the parietal pericardium are susceptible to chemical stimulation. Bradykinin is a powerful algesic agent and is formed and released locally during inflammation. We suggest, therefore, that the pericardial sympathetic pressor reflex is nociceptive in nature and can be activated when kinin formation occurs during pericardial inflammation.

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