Antagonistic Interaction Between BIIE 0246, a Neuropeptide Y Y2-Receptor Antagonist, and .OMEGA.-Conotoxin GVIA, a Ca2+ Channel Antagonist, in Presynaptic Transmitter Releases in Dog Splenic Arteries.

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  • Antagonistic Interaction Between BIIE 0246, a Neuropeptide Y Y2-Receptor Antagonist, and ω-Conotoxin GVIA, a Ca2+ Channel Antagonist, in Presynaptic Transmitter Releases in Dog Splenic Arteries
  • Antagonistic Interaction Between BIIE 0246 a Neuropeptide Y Y2 Receptor Antagonist and オメガ Conotoxin GVIA a Ca2 Channel Antagonist in Presynaptic Transmitter Releases in Dog Splenic Arteries
  • Antagonistic Interaction Between BIIE 0246, a Neuropeptide Y Y2-Receptor Antagonist, and ωy-Conotoxin GVIA, a Ca2+ Channel Antagonist, in Presynaptic Transmitter Releases in Dog Splenic Arteries

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Abstract

Isolated dog splenic arteries were perfused with Krebs-Henseleit solution at 37°C, using the cannula inserting method. Periarterial nerve electrical stimulation (10-V amplitude; 1-ms duration; 30-s trains of pulses; 1, 4 and 10 Hz) readily caused double peaked vasoconstrictions, i.e., 1st peaked response was mostly inhibited by α,β-methylene ATP and the 2nd one, by prazosin. These responses were consistently inhibited by ω-conotoxin GVIA (ω-CTX), whereas they were facilitated by BIIE 0246, a neuropeptide Y (NPY) Y2-receptor antagonist. The ω-CTX-induced blocking effects of transmitter release were significantly antagonized by BIIE 0246. It is possible that the NPY Y2 receptor activity may partially be linked to presynaptic Ca2+ channels.

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