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自发性高血压大鼠对毒扁豆碱的升压反应增强。

Increased pressor responses to physostigmine in spontaneously hypertensive rats.

作者信息

Kubo T, Tatsumi M

出版信息

Naunyn Schmiedebergs Arch Pharmacol. 1979 Jan;306(1):81-3. doi: 10.1007/BF00515597.

Abstract

Intravenous injection of physostigmine evoked a pressor response in unanaesthetized rats. Spontaneously hypertensive rats (SHR) showed increased pressor responses, but the responses were within normal limits in renal hypertensive and DOCA-saline hypertensive rats. The pressor effect in SHR was abolished by the i.v. injection of atropine sulphate but not by the i.v. injection of atropine methylbromide. After inhibition of the peripheral muscarinic receptors by atropine methyl bromide, oxotremorine also produced a pressor response in unanaesthetized rats. In contrast to the pressor effect of physostigmine, there was no difference between the oxotremorine-induced pressor response of SHR and that of normotensive Wistar-Kyoto rats. The pressor effect of oxotremorine in SHR was blocked by the i.v. injection of atropine sulphate.

摘要

静脉注射毒扁豆碱可在未麻醉大鼠中引发升压反应。自发性高血压大鼠(SHR)的升压反应增强,但肾性高血压大鼠和去氧皮质酮-盐水性高血压大鼠的反应在正常范围内。SHR中的升压作用可通过静脉注射硫酸阿托品消除,但不能通过静脉注射甲基溴化阿托品消除。在甲基溴化阿托品抑制外周毒蕈碱受体后,氧化震颤素也能在未麻醉大鼠中产生升压反应。与毒扁豆碱的升压作用相反,SHR和正常血压的Wistar-Kyoto大鼠对氧化震颤素诱导的升压反应没有差异。SHR中氧化震颤素的升压作用可被静脉注射硫酸阿托品阻断。

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