MODULATION OF CALCITONIN-GENE-RELATED PEPTIDE RELEASE EVOKED BY BRADYKININ AND ELECTRICAL-FIELD STIMULATION IN GUINEA-PIG ATRIA

Electrical field stimulation (EFS) and bradykinin (BK) are able to activate capsaicin-sensitive sensory neurons of guinea-pig atria in a omega-conotoxin (CTX)-sensitive and Ruthenium Red (RR)-insensitive manner. The aim of this work was to study EFS and BK-induced release of calcitonin gene-related peptide (CGRP) from guinea-pig atria and in particular the action of morphine and neuropeptide Y (NPY) on this release. EFS-induced CGRP release was frequency-dependent and tetrodotoxin (TTX)-sensitive, while BK-evoked CGRP release was TTX-insensitive. On the other hand, CGRP outflow induced by either EFS or BK was similarly reduced in the presence of morphine and NPY. It is therefore hypothesized that NPY and opioids exert their inhibitory action by acting on the very terminal region of the nerve fibre. Moreover, our results show that dermorphine but not dynorphin reduced BK-evoked CGRP release, suggesting that mu opioid receptors are responsible for morphine action. Studying the action of peptide W and NPY(16-36) on BK-evoked CGRP release, we demonstrated that both had similar inhibitory effects, supporting the presence of Y, receptors on the nerve terminal region.