Studies of reflexogenic effects of capsaicin and neuropeptides on neural afferents in the dog parietal pericardium.

Stimulation of neural afferents in the parietal pericardium of anaesthetized, open-chest dogs by local application of capsaicin (0.1-100 micrograms) consistently induced dose-related pressor effects and tachycardia, whereas the application (0.1-1 microgram) of neuropeptides substance P (SP), neurokinin A (NKA), neurokinin B (NKB) or calcitonin gene-related peptide (CGRP) had no cardiovascular effect. Capsaicin-induced reflex responses were not affected by vagotomy, but were abolished by bilateral sectioning of the upper thoracic (T1-T4) white rami communicantes and stellectomy. Capsaicin-induced reflex tachycardia could also be abolished by a beta-adrenoceptor blockade with propranolol (0.5 mg/kg, IV), while ganglionic blockade with pentolinium (0.5 mg/kg, IV) eliminated both the tachycardia and pressor effects. Intravenous treatment with the cyclo-oxygenase inhibitors, indomethacin (5 mg/kg) or aspirin (100 mg/kg) had no effect on reflex pressor and heart rate responses to pericardial capsaicin. Also local treatment of the pericardium with either indomethacin (1 microgram/ml) or dual cyclooxygenase/lipoxygenase inhibitor, BW755C (10 micrograms/ml) failed to affect the responses to capsaicin. We conclude that (i) capsaicin-sensitive afferents which are present in the dog pericardium have a spinal origin and can initiate sympathetically-mediated reflex cardiovascular changes; (ii) the reflexogenic action of capsaicin on pericardial afferents does not depend on local production of eicosanoids; (iii) neuropeptides appear to be without reflexogenic effects on neural afferents in the dog parietal pericardium.