百日咳毒素可阻断卡巴胆碱的致渴作用，但不阻断血管紧张素II的致渴和升压作用。
Pertussis toxin blocks the dipsogenic actions of carbachol, but does not block the dipsogenic and pressor actions of angiotensin II.
作者信息
Speth R C, Grove K L
机构信息
Department of Veterinary and Comparative Anatomy, Pharmacology and Physiology, Washington State University, Pullman 99164-6520.
出版信息
Regul Pept. 1991 Feb 1;32(2):121-8. doi: 10.1016/0167-0115(91)90040-n.
Rats were tested for dipsogenic and pressor responses to intracerebroventricularly (icv) administered Ang II and for dipsogenic responses to icv administered carbachol in the absence and presence of pertussis toxin, also administered icv. Pertussis toxin did not inhibit the pressor or dipsogenic responses to Ang II, but did inhibit the dipsogenic responses to carbachol. This suggests that the pressor and dipsogenic responses to Ang II in the brain are not mediated by a pertussis toxin-sensitive G protein, but that the muscarinic cholinergic dipsogenic response is mediated by a pertussis toxin-sensitive G protein.
对大鼠进行如下实验
检测其对脑室内（icv）注射血管紧张素II（Ang II）的致渴和升压反应，以及在不存在和存在同样经icv注射的百日咳毒素的情况下，对icv注射卡巴胆碱的致渴反应。百日咳毒素并未抑制对Ang II的升压或致渴反应，但确实抑制了对卡巴胆碱的致渴反应。这表明，大脑中对Ang II的升压和致渴反应不是由对百日咳毒素敏感的G蛋白介导的，而毒蕈碱胆碱能致渴反应是由对百日咳毒素敏感的G蛋白介导的。
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