{"title":"神经肽yy2受体拮抗剂BIIE 0246和Ca2+通道拮抗剂omega- concontoxin GVIA在狗脾动脉突触前递质释放中的拮抗相互作用","authors":"Xiao‐ping Yang, S. Chiba","doi":"10.1254/JJP.89.188","DOIUrl":null,"url":null,"abstract":"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.","PeriodicalId":14750,"journal":{"name":"Japanese journal of pharmacology","volume":"22 1","pages":"188-91"},"PeriodicalIF":0.0000,"publicationDate":"2002-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"3","resultStr":"{\"title\":\"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.\",\"authors\":\"Xiao‐ping Yang, S. Chiba\",\"doi\":\"10.1254/JJP.89.188\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"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.\",\"PeriodicalId\":14750,\"journal\":{\"name\":\"Japanese journal of pharmacology\",\"volume\":\"22 1\",\"pages\":\"188-91\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2002-06-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"3\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Japanese journal of pharmacology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1254/JJP.89.188\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Japanese journal of pharmacology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1254/JJP.89.188","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
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.
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