Abstract
The effect of superfusion with veratridine on the release of calcitonin gene-related peptide-like immunoreactivity (CGRP-LI) was studied in slices of rat urinary bladder. Exposure to veratridine (1–200 μM) produced a concentration-related release of CGRP-LI. Veratridine (50 μM)-evoked CGRP-LI release was abolished in slices pre-exposed to capsaicin (10 μM for 40 min) or superfused in a Ca 2+-free medium containing 1 mM EDTA. After exposure to veratridine (50 μM for 40 min), capsaicin (10 μM) was still able to release CGRP-LI. CGRP-LI release evoked by veratridine (50 μM) was inhibited by about 60% by tetrodotoxin (0,3 μM), attenuated (30%) by nifedipine (1 μM), and not affected by ω-conotoxin (0.1 μM). The capsaicin antagonist ruthenium red (10 μM) did not affect veratridine (50 μM)-evoked CGRP-LI release. The present results indicate that depolarization by veratridine induces CGRP-LI release from capsaicin-sensitive nerve fibres, an effect that is entirely dependent on extracellular Ca 2+. The Ca 2+ influx that promotes CGRP-LI release is mediated mostly by nifedipine-, ω-conotoxin- and ruthenium red-insensitive channels.
Published Version
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