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.
Isolated dog splenic arteries were perfused with Krebs-Henseleit solution at 37 degrees 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 alpha,beta-methylene ATP and the 2nd one, by prazosin. These responses were consistently inhibited by omega-conotoxin GVIA (omega-CTX), whereas they were facilitated by BIIE 0246, a neuropeptide Y (NPY) Y2-receptor antagonist. The omega-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.
Yang
Xiao-Ping
XP
Department of Pharmacology, Shinshu University School of Medicine, Matsumoto, Japan.
Chiba
Shigetoshi
S
D000818:Animals; D001120:Arginine / Q000031:analogs & derivatives* / Q000494:pharmacology*; D001552:Benzazepines / Q000494:pharmacology*; D002121:Calcium Channel Blockers / Q000494:pharmacology*; D004285:Dogs; D004558:Electric Stimulation; D005260:Female; D066298:In Vitro Techniques; D008297:Male; D018377:Neurotransmitter Agents / Q000378:metabolism*; D017729:Presynaptic Terminals / Q000187:drug effects* / Q000378:metabolism / Q000502:physiology; D017476:Receptors, Neuropeptide Y / Q000037:antagonists & inhibitors*; D013157:Splenic Artery / Q000187:drug effects* / Q000378:metabolism / Q000502:physiology; D014661:Vasoconstriction / Q000187:drug effects; D020866:omega-Conotoxin GVIA / Q000494:pharmacology*
D001552:Benzazepines; D002121:Calcium Channel Blockers; D018377:Neurotransmitter Agents; D017476:Receptors, Neuropeptide Y; C095889:neuropeptide Y2 receptor; D020866:omega-Conotoxin GVIA; D001120:Arginine; C403256:BIIE 0246