Abstract
Both bradykinin and capsaicin infusion evoked a marked increase in the outflow of substance P- (SP-LI) and calcitonin gene-related peptide-like immunoreactivity (CGRP-LI) from guinea-pig isolated, perfused heart. After acute exposure to capsaicin in vitro, or in hearts taken from animals pretreated in vivo with capsaicin, bradykinin failed to induce any release. The positive chronotropic effect of bradykinin was reduced after acute capsaicin administration. The effect of bradykinin in the guinea-pig heart could be mediated, at least partly, by release of neuropeptides from peripheral endings of capsaicin-sensitive sensory neurones.
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