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氧化震颤素和槟榔碱激动唾液腺Ｍ受体剂量依赖性地诱发小鼠流涎，ＥＤ＿（５０）值分别为１１６．２７±２０．１１μｇ／ｋｇｓｃ和９．０２±１．７５ｍｇ／ｋｇｓｃ。烟碱（０．５，１．０ｍｇ／ｋｇｓｃ间隔５ｍｉｎ）预处理后，氧化震颤素和槟榔碱诱发小鼠流涎作用的量效曲线显著左移，ＥＤ＿（５０）值分别降为４３．２５±１１．５２μｇ／ｋｇｓｃ和４．７５±０．７６ｍｇ／ｋｇｓｃ。以美加明阻断Ｎ受体功能后，能对抗烟碱调节Ｍ受体激动剂的流涎作用。以氯化锂抑制肌醇磷酸酶后，能增强烟碱调节Ｍ激动剂的流涎作用。提示烟碱增强唾液腺Ｍ受体对其激动剂的反应性和敏感性，可能与神经元性Ｎ受体干扰唾液腺磷脂酰肌醇代谢有关。
Oxalotoxin and arecoline stimulated salivary gland M receptor dose-dependently induced mouse salivation, ED 50 values were 116.27 ± 20.11μg / kgsc and 9.02 ± 1.75mg / kgsc respectively. Nicotine (0.5,1.0mg / kgsc interval 5min) pretreatment, the oxidation of tremor and arecoline-induced salivation in mice dose-response curve significantly shifted to the left, ED 50 values were reduced to 43.25 ± 11.52 μg / kgsc and 4.75 ± 0.76 mg / kgsc. With Mecamin blocked N receptor function, nicotine can regulate the M receptor agonist salivation effect. Lithium chloride inhibition of inositol phosphatase, nicotine can enhance the modulation of M agonist salivation effect. It is suggested that nicotine may enhance the reactivity and sensitivity of M receptor to its agonist, which may be related to the interference of neuronal N receptor with phosphatidylinositol metabolism in salivary gland.