Evidence for two independent modes of activation of the 'efferent' function of capsaicin-sensitive nerves.

Field stimulation (10 Hz for 10 s, 0.5 ms pulse width, 60 V) of the guinea-pig isolated main bronchi (atropine plus indomethacin in the bath) produced reproducible contractions which were abolished by tetrodotoxin or in vitro capsaicin desensitization. These responses were almost abolished by omega-conotoxin GVIA (CTX), a peptide modulator of neuronal calcium channels which, however, did not affect the bronchial contraction due to neurokinin A or to capsaicin. Field stimulation (10 Hz for 2.5 s, 1 ms, 60 V) of the electrically driven, isolated guinea-pig left atria excised from reserpine-pretreated animals (atropine in the bath) produced a delayed positive inotropic response which was abolished by tetrodotoxin or in vitro capsaicin desensitization. This response was abolished by CTX, which did not affect the response to exogenous calcitonin gene-related peptide nor that to capsaicin. These findings indicate that CTX-sensitive mechanisms (presumably Ca channels regulating the release of transmitters) are activated upon antidromic invasion of sensory terminals and consequent production of the 'efferent' response while the activation of sensory nerve endings by capsaicin occurs through CTX-resistant mechanisms.