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2
Bovine isolated middle cerebral artery contractions to antimigraine drugs.牛离体大脑中动脉对抗偏头痛药物的收缩反应。
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3
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Br J Pharmacol. 1999 Nov;128(6):1133-40. doi: 10.1038/sj.bjp.0702773.
4
5-Hydroxytryptamine(1F) receptors do not participate in vasoconstriction: lack of vasoconstriction to LY344864, a selective serotonin(1F) receptor agonist in rabbit saphenous vein.5-羟色胺（1F）受体不参与血管收缩：兔隐静脉对选择性5-羟色胺（1F）受体激动剂LY344864无血管收缩反应。
J Pharmacol Exp Ther. 1999 Sep;290(3):935-9.
5
Coronary side-effect potential of current and prospective antimigraine drugs.当前及未来抗偏头痛药物的冠状动脉副作用可能性
Circulation. 1998 Jul 7;98(1):25-30. doi: 10.1161/01.cir.98.1.25.
6
SB-216641 and BRL-15572--compounds to pharmacologically discriminate h5-HT1B and h5-HT1D receptors.SB - 216641和BRL - 15572——用于从药理学上区分h5 - HT1B和h5 - HT1D受体的化合物。
Naunyn Schmiedebergs Arch Pharmacol. 1997 Sep;356(3):312-20. doi: 10.1007/pl00005056.
7
Allosteric equilibrium model explains steady-state coupling of beta-adrenergic receptors to adenylate cyclase in turkey erythrocyte membranes.变构平衡模型解释了火鸡红细胞膜中β-肾上腺素能受体与腺苷酸环化酶的稳态偶联。
Biochem J. 1997 May 1;323 ( Pt 3)(Pt 3):765-76. doi: 10.1042/bj3230765.
8
Recombinant saphenous vein 5-HT1B receptors of the rabbit: comparative pharmacology with human 5-HT1B receptors.兔重组隐静脉5-HT1B受体：与人5-HT1B受体的比较药理学
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9
Evidence for 5-HT1D beta but not 5-HT1D alpha receptor subtype expression in canine large coronary arteries and saphenous vein.犬大冠状动脉和隐静脉中存在5-HT1Dβ受体亚型表达，但不存在5-HT1Dα受体亚型表达的证据。
Cardiovasc Res. 1996 May;31(5):793-9. doi: 10.1016/0008-6363(96)00014-4.
10
Selective antagonism of human 5-HT1D and 5-HT1B receptor-mediated responses in stably transfected C6-glial cells by ketanserin and GR 127,935.酮色林和GR 127,935对稳定转染的C6神经胶质细胞中人5-HT1D和5-HT1B受体介导反应的选择性拮抗作用。
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激动剂导向的转运解释了那拉曲普坦和舒马曲坦在兔颈总动脉中反应模式的差异。

Agonist-directed trafficking explaining the difference between response pattern of naratriptan and sumatriptan in rabbit common carotid artery.

作者信息

Akin Demet, Onaran H Ongun, Gurdal Hakan

机构信息

Department of Pharmacology and Clinical Pharmacology, Medical Faculty of Ankara University, Sihhiye, Ankara 06100 Turkey.

出版信息

Br J Pharmacol. 2002 May;136(2):171-6. doi: 10.1038/sj.bjp.0704710.

DOI:10.1038/sj.bjp.0704710
PMID:12010764
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1573348/
Abstract
  1. Sumatriptan or eletriptan produced vasocontraction in common carotid artery (CCA) by stimulating 5HT(1B) receptors (see also Akin & Gurdal, this issue). 2. Naratriptan as a 5HT(1B/D) agonist, was unable to produce vasocontraction in this artery, but inhibited the vasocontractile response induced by sumatriptan or eletriptan. 3. All these agonists inhibited forskolin-stimulated cyclic AMP production with comparable potencies and maximal responses. This inhibition was mediated by 5HT(1B) receptors: 5HT(1B) antagonist SB216641 (1 microM) completeley antagonized sumatriptan-, eletriptan- or naratriptan-induced cyclic AMP inhibition, but 5HT(1D) antagonist BRL15572 (1 microM) did not affect this response. 4. Naratriptan-induced stimulation of 5-HT(1B) receptors resulted only in adenylate cyclase inhibition, whereas stimulation of these receptors by sumatriptan or eletriptan produced vasocontraction as well. Hence, we concluded that the 5HT(1B)-mediated inhibition of adenylate cyclase was not a sufficient condition to couple the receptor stimulation to vasocontraction. 5. We discussed agonist-induced trafficking as a plausible mechanism for the observed phenomenon.
摘要
  1. 舒马曲坦或依来曲坦通过刺激5HT(1B)受体，使颈总动脉（CCA）产生血管收缩（另见本期Akin和Gurdal的文章）。2. 那拉曲坦作为一种5HT(1B/D)激动剂，无法使该动脉产生血管收缩，但能抑制舒马曲坦或依来曲坦诱导的血管收缩反应。3. 所有这些激动剂均以相当的效力和最大反应抑制福斯高林刺激的环磷酸腺苷（cAMP）生成。这种抑制作用由5HT(1B)受体介导：5HT(1B)拮抗剂SB216641（1微摩尔）完全拮抗舒马曲坦、依来曲坦或那拉曲坦诱导的环磷酸腺苷抑制作用，但5HT(1D)拮抗剂BRL15572（1微摩尔）对此反应无影响。4. 那拉曲坦诱导的5-HT(1B)受体刺激仅导致腺苷酸环化酶抑制，而舒马曲坦或依来曲坦对这些受体的刺激则同时产生血管收缩。因此，我们得出结论，5HT(1B)介导的腺苷酸环化酶抑制并非将受体刺激与血管收缩偶联的充分条件。5. 我们讨论了激动剂诱导的转运作为所观察现象的一种可能机制。