Palov O G, Ovsiannikov V I
Fiziol Zh SSSR Im I M Sechenova. 1988 Mar;74(3):404-13.
In anesthetized cats with i. a. perfusion of isolated small intestine segments, the blockade of N-cholinoreceptors with benzohexonium of M-cholinoreceptors with atropine reduced jejunum and ileum contractility induced by bradykinin. After an alpha-adrenoreceptor blockade induced by phentolamine, an increase of responsiveness to bradykinin was evident whereas noradrenaline stimulation reduced the contractility. The blockade of beta-adrenoreceptors with propranolol as well as their stimulation with isopropylnoradrenaline also reduced small intestine contractility. The bradykinin-induced contractions of the small intestine segments seem to be due to the direct action of bradykinin on the smooth muscle cells and to the stimulating effect of acetylcholine released from the efferent cholinergic neurons. These effects can be modulated with catecholamine because of its influence on the excitatory presynaptic beta-adrenoreceptors and inhibitory postsynaptic alpha- and beta-adrenoreceptors.
在对麻醉猫进行分离小肠段的动脉内灌注时,用苯磺铵阻断N - 胆碱受体以及用阿托品阻断M - 胆碱受体可降低缓激肽诱导的空肠和回肠收缩性。在用酚妥拉明诱导α - 肾上腺素受体阻断后,对缓激肽的反应性明显增加,而去甲肾上腺素刺激则降低收缩性。用普萘洛尔阻断β - 肾上腺素受体以及用异丙去甲肾上腺素刺激它们也会降低小肠收缩性。小肠段缓激肽诱导的收缩似乎是由于缓激肽对平滑肌细胞的直接作用以及传出胆碱能神经元释放的乙酰胆碱的刺激作用。由于儿茶酚胺对兴奋性突触前β - 肾上腺素受体以及抑制性突触后α - 和β - 肾上腺素受体的影响,这些作用可被儿茶酚胺调节。