Abstract
Hypertonic NaCl (160 mM added to the physiological salt solution) releases CGRP in a Ca(2+)-dependent manner from capsaicin-sensitive sensory nerves of the rat urinary bladder. The NaCl (160 mM)-evoked CGRP release was not affected by tetrodotoxin (0.3 microM), nifedipine (1 microM), omega-conotoxin (0.1 microM) and ruthenium red (10 microM). NaCl (160 mM)-evokes release of sensory neuropeptides without the involvement of axon reflexes, and by promoting Ca2+ influx via a dihydropyridine omega-conotoxin and ruthenium red insensitive pathway.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Animals
-
Calcitonin Gene-Related Peptide / drug effects*
-
Calcitonin Gene-Related Peptide / metabolism
-
Calcium Channel Blockers / pharmacology*
-
In Vitro Techniques
-
Male
-
Nifedipine / pharmacology
-
Peptides, Cyclic / pharmacology
-
Rats
-
Rats, Inbred Strains
-
Ruthenium Red / pharmacology
-
Saline Solution, Hypertonic / pharmacology*
-
Tetrodotoxin / pharmacology*
-
omega-Conotoxins*
Substances
-
Calcium Channel Blockers
-
Peptides, Cyclic
-
Saline Solution, Hypertonic
-
omega-Conotoxins
-
Conus magus toxin
-
Ruthenium Red
-
Tetrodotoxin
-
Nifedipine
-
Calcitonin Gene-Related Peptide