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首页> 外文期刊>Life sciences >Pharmacological analysis of the mechanisms involved in the tachycardic and vasopressor responses to the antimigraine agent, isometheptene, in pithed rats.
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Pharmacological analysis of the mechanisms involved in the tachycardic and vasopressor responses to the antimigraine agent, isometheptene, in pithed rats.

机译：对成年大鼠对抗偏头痛药异丁烯对心动过速和升压药反应的机制的药理分析。

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The present study set out to investigate the pharmacological profile of the cardiovascular responses induced by the antimigraine agent, isometheptene, in pithed rats. For this purpose, intravenous (i.v.) administration of blocking doses of the antagonists prazosin (alpha1; 100 microg/kg), rauwolscine (alpha2; 300 microg/kg), the combination of prazosin (100 microg/kg) plus rauwolscine (300 microg/kg), propranolol (beta; 1000 microg/kg), ritanserin (5-HT2; 100 microg/kg) or equivalent volumes of saline (1 ml/kg) were used. Isometheptene (0.03, 0.1, 0.3, 1 and 3 mg/kg, i.v.) produced dose-dependent increases in heart rate and diastolic blood pressure which were highly reproducible as they remained unaltered after saline. These tachycardic responses to isometheptene remained unaffected after prazosin, rauwolscine, ritanserin or the combination prazosin plus rauwolscine, but were abolished after propranolol. In contrast, the isometheptene-induced vasopressor responses were not significantly modified after the above doses of rauwolscine, ritanserin or propranolol, but were markedly blocked after prazosin or the combination of prazosin plus rauwolscine; the latter blockade did not significantly differ from that produced by prazosin alone. Interestingly, in rats pretreated intraperitoneally (i.p.) with reserpine (5 mg/kg; -24 h), isometheptene-induced tachycardic responses were abolished whereas the corresponding vasopressor responses were markedly attenuated and subsequently blocked by prazosin. It is concluded that isometheptene-induced tachycardic responses seem to involve only an indirect (tyramine-like action) mechanism mediated by beta-adrenoceptors, whilst the corresponding vasopressor responses are mediated by a predominantly indirect (tyramine-like action), as well as a minor direct (alpha1-adrenoceptors), sympathomimetic mechanism.
机译：本研究着手研究抗偏头痛药物异甲基庚烯在有髓大鼠中引起的心血管反应的药理学特征。为此，静脉内（iv）给予阻断剂量的拮抗剂哌唑嗪（α1; 100微克/千克），劳沃辛（α2; 300微克/千克），哌唑嗪（100微克/千克）加劳伍辛（300微克）的联合剂量使用了心得安（β; 1000微克/千克），利坦色林（5-HT2; 100微克/千克）或等体积的盐水（1毫升/千克）。异美汀（0.03、0.1、0.3、1和3 mg / kg，静脉内）产生剂量依赖性的心率和舒张压升高，由于在盐水中保持不变，因此可高度重现。这些对异丁烯的心动过速反应在哌唑嗪，劳劳斯金，利坦色林或哌唑嗪加劳伍斯金的组合后均不受影响，但在普萘洛尔后被取消。相比之下，在上述剂量的劳沃辛，利坦色林或普萘洛尔使用上述剂量后，异丁烯诱导的血管升压反应没有明显改变，但是在哌唑嗪或吡唑嗪与劳沃辛组合后明显被阻断。后者的阻断作用与单独使用哌唑嗪所产生的阻断作用没有显着差异。有趣的是，在大鼠腹膜内（i.p.）利血平（5 mg / kg; -24 h）预处理的大鼠中，异丁烯诱导的心动过速反应被消除，而相应的升压药反应显着减弱，随后被哌唑嗪阻断。结论是异丁烯诱导的心动过速反应似乎仅涉及由β-肾上腺素受体介导的间接（酪胺样作用）机制，而相应的血管加压药反应则主要由间接（酪胺样作用）介导。次要直接作用（α1-肾上腺素受体），拟交感神经机制。

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