Abstract
The aim of this study was to characterise the release of calcitonin gene-related peptide (CGRP) by capsaicin, low pH and prostacyclin in terms of Ca 2+ channel dependence, interactions with K ATP channels and the role of action potential propagation, in the isolated, perfused guinea-pig heart. The Ca 2+ channel blocker ω-conotoxin reduced CGRP release evoked by 10 −7 M capsaicin, as well as CGRP release evoked by pH 7. CGRP release caused by capsaicin at low (10 −7 M) but not high (10 −6 M) concentrations was also attenuated by tetrodotoxin, indicating partial dependence on action potential propagation. CGRP release caused by prostacyclin was not altered by any of the tested drugs. The K ATP channel activator cromakalim and the K ATP channel blocker glibenclamide had no effect on CGRP release. Previous findings that low pH and capsaicin stimulate capsaicin-sensitive afferents in the isolated heart at least partly through common mechanisms are thus supported. Attenuation of capsaicin-evoked release of CGRP by tetrodotoxin suggests recruitment of additional nerve terminals by a local axon reflex.
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