Reflex effects evoked from the parietal pericardium in the dog: comparison with responses from the visceral pericardium.

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.