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• W2154150489 startingPage "G1027" @default.
• W2154150489 abstract "In enteric synaptosomes of the rat, the role of voltage-dependent Ca 2+ 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 Ca 2+ 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) Ca 2+ 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 (Ni 2+ , 10 −6 M) Ca 2+ channels. In contrast, NO synthesis was suppressed by ω-agatoxin-IVA, ω-conotoxin-GVIA, and isradipine by ∼79, 70, and 70%, respectively, whereas Ni 2+ 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 Ca 2+ channels, whereas NO synthesis is presumably dependent on Ca 2+ influx not only via the P- and N- but also via the L-type Ca 2+ channel. In contrast, none of the Ca 2+ channel blockers affected VIP release evoked by exogenous NO, suggesting that NO induces VIP secretion by a different mechanism, presumably involving intracellular Ca 2+ stores." @default.
• W2154150489 created "2016-06-24" @default.
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• W2154150489 date "2002-11-01" @default.
• W2154150489 modified "2023-09-27" @default.
• W2154150489 title "Characterizing voltage-dependent Ca2+ channels coupled to VIP release and NO synthesis in enteric synaptosomes" @default.
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• W2154150489 doi "https://doi.org/10.1152/ajpgi.00400.2001" @default.
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