Release of sensory CGRP by hypertonic NaCl is not blocked by tetrodotoxin, omega-conotoxin, nifedipine and ruthenium red

Life Sci. 1992;51(8):PL73-6. doi: 10.1016/0024-3205(92)90234-g.

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