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首页> 外文期刊>Life sciences >PRESSOR EFFECT OF THE PUTATIVE M(1) MUSCARINIC RECEPTOR AGONIST MCN-A-343 IN THE CONSCIOUS RAT
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PRESSOR EFFECT OF THE PUTATIVE M(1) MUSCARINIC RECEPTOR AGONIST MCN-A-343 IN THE CONSCIOUS RAT

机译：潜伏性大鼠中M（1）肌肉受体激动剂MCN-A-343的加压作用

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The putative M(1) muscarinic receptor agonist McN-A-343 evoked a dose-dependent increase in mean arterial pressure (MAP) when administered intravenously to conscious freely-moving rats pretreated with the ganglionic nicotinic receptor antagonist pentolinium. A tachycardia accompanied the increase in MAP which was blocked by the beta-adrenergic receptor antagonist propranolol. The increase in MAP was attenuated by the alpha(1)-adrenergic receptor antagonist prazosin combined with the alpha(2)-adrenergic receptor antagonist yohimbine. Adding propranolol to alpha-adrenergic receptor blockade uncovered a latent presser response. Replacing prazosin with benextramine (which blocks NPY in addition to alpha-adrenergic receptors) attenuated the presser response unmasked by propranolol. This attenuation was comparable to that provided by benextramine of the presser response to intravenous administration of NPY. Adrenal demedullation only slightly attenuated the presser response while having no effect on the tachycardia. The catecholamine depletor guanethidine greatly attenuated the McN-A-343-evoked increase in MAP and heart rate. The combination of adrenal demedullation and guanethidine did not further attenuate the increase in MAP but did provide better attenuation of the tachycardia than guanethidine alone. These results show that McN-A-343 evokes an increase in MAP and heart rate of conscious freely-moving rats primarily by causing the release of catecholamines, and possibly NPY, from sympathetic neurons with the adrenal glands playing a minor role. [References: 33]
机译：推定的M（1）毒蕈碱受体激动剂McN-A-343在静脉注射给用神经节烟碱受体拮抗剂戊脑预处理的有意识的自由运动大鼠时，引起平均动脉压（MAP）的剂量依赖性增加。心动过速伴有MAP升高，后者被β-肾上腺素能受体拮抗剂普萘洛尔阻断。 MAP的增加被与α（2）-肾上腺素受体拮抗剂育亨宾联合的α（1）-肾上腺素受体拮抗剂哌唑嗪减弱了。将普萘洛尔添加到α-肾上腺素受体阻滞剂中发现潜在的升压反应。用苯达曲明代替哌唑嗪（除α-肾上腺素受体外还阻断NPY）减弱了普萘洛尔掩盖的升压反应。这种衰减与苯丙胺对静脉注射NPY的升压反应产生的衰减相当。肾上腺去髓质仅轻微地降低了升压反应，而对心动过速没有影响。儿茶酚胺耗竭剂胍乙啶极大地减弱了McN-A-343引起的MAP和心率增加。肾上腺髓质脱质和胍乙胺的结合并没有进一步减弱MAP的增加，但是确实比单独的胍乙啶提供了更好的心动过速的减轻。这些结果表明，McN-A-343主要通过引起交感神经元释放儿茶酚胺和可能的NPY来引起有意识自由运动大鼠的MAP和心率增加，而肾上腺的作用较小。 [参考：33]

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