Mechanism of nitric oxide-induced contraction in the rat isolated small intestine

R. A. Lefebvre, L. Bartho

Research output: Contribution to journalArticle

25 Citations (Scopus)

Abstract

1. The contractile response to nitric oxide (NO) in ral ileal myenteric plexus-longitudinal muscle strips was pharmacologically analysed. 2. NO (10-7 M) induced only contraction while 10-6 M NO induced contraction followed by relaxation. Methylene blue (up to 10-4 M) did not affect the NO-induced contractions but significantly reduced the relaxation evoked by 10-6 M NO. Administration of 8-bromo-cyclic GMF (10-6-10-4 M) only induced relaxation. 3. Sodium nitroprusside (SNF; 10-7-10-5 M) induced concentration-dependent contractions per se; the contractile response to NO, administered within 10 min after SNP, was concentration-dependently reduced. The guanosine 3':5'-cyclic monophosphate (cyclic GMP) content of the tissues was not increased during contractions with 10-8 M NO and 10-6 M SNP; it was increased by a factor of 2 during contraction with 10-7 M NO, and by a factor of 12 during relaxation with 3 x 10-6 M NO. 4. The NO-induced contractions were not affected by ryanodine (3 x 10-5 M) but were concentration-dependently reduced by nifedipine (10-8-10-7 M) and apamin (3 x 10-9-3 x 10-8 M). 5. These results suggest that cyclic GMP is not involved in the NO-induced contraction in the rat small intestine. The NO-induced contraction is related to extracellular Ca2+ influx through L-type Ca2+ channels, that might be activated in response to the closure of Ca2+-dependent K+ channels.

Original languageEnglish
Pages (from-to)975-981
Number of pages7
JournalBritish journal of pharmacology
Volume120
Issue number5
DOIs
Publication statusPublished - 1997

Keywords

  • Ca channels
  • K channels
  • Nitric oxide (NO)
  • Small intestine

ASJC Scopus subject areas

  • Pharmacology

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