Characterizing voltage-dependent Ca2+ channels coupled to VIP release and NO synthesis in enteric synaptosomes

Manfred Kurjak, A. Sennefelder, M. Aigner, V. Schusdziarra, H. D. Allescher

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8 Scopus citations


In enteric synaptosomes of the rat, the role of voltage-dependent Ca2+ channels in K+-induced VIP release and nitric oxide (NO) synthesis was investigated. Basal VIP release was 39 ± 4 pg/mg, and cofactor-substituted NO synthase activity was 7.0 ± 0.8 fmol·mg-1·min-1. K+ depolarization (65 mM) stimulated VIP release Ca2+ dependently (basal, 100%; K+, 172.2 ± 16.2%; P < 0.05, n = 5). K+-stimulated VIP release was reduced by blockers of the P-type (ω-agatoxin-IVA, 3 × 10-8 M) and N-type (ω-conotoxin-GVIA, 10-6 M) Ca2+ channels by ∼50 and 25%, respectively, but not by blockers of the L-type (isradipine, 10-8 M), Q-type (ω-conotoxin-MVIIC, 10-6 M), or T-type (Ni2+, 10-6 M) Ca2+ channels. In contrast, NO synthesis was suppressed by ω-agatoxin-IVA, ω-conotoxin-GVIA, and isradipine by ∼79, 70, and 70%, respectively, whereas Ni2+ and ω-conotoxin-MVIIC had no effect. These findings are suggestive of a coupling of depolarization-induced VIP release primarily to the P- and N-type Ca2+ channels, whereas NO synthesis is presumably dependent on Ca2+ influx not only via the P- and N- but also via the L-type Ca2+ channel. In contrast, none of the Ca2+ channel blockers affected VIP release evoked by exogenous NO, suggesting that NO induces VIP secretion by a different mechanism, presumably involving intracellular Ca2+ stores.

Original languageEnglish
Pages (from-to)G1027-G1034
JournalAmerican Journal of Physiology - Gastrointestinal and Liver Physiology
Issue number5 46-5
StatePublished - Nov 2002


  • Enteric nervous system
  • Nitric oxide synthase
  • Synaptosomes
  • Vasoactive intestinal polypeptide
  • Voltage-dependent Ca channels


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