Sayardoust Shariel, Ekström Jörgen
Department of Pharmacology, Sahlgrenska Academy at Göteborg University, Medicinaregatan 15 D, P.O. Box 431, 413 90 Göteborg, Sweden.
Arch Oral Biol. 2006 Mar;51(3):189-97. doi: 10.1016/j.archoralbio.2005.07.004. Epub 2005 Sep 6.
Incorporation of radiolabelled leucine and thymidine into trichloroacetic acid-insoluble material of the parotid gland was used as indices of protein synthesis and mitotic activity, respectively, following electrical stimulation of the parasympathetic auriculo-temporal nerve for 30 min in pentobarbitone-anaesthetized rats under adrenoceptor blockade (phentolamine and propranolol, 2mg/kg intravenous of each) in the absence or presence of atropine (2mg/kg intravenous) and without or with nitric oxide synthase inhibitors. In atropinized rats, the parasympathetic non-adrenergic, non-cholinergic (NANC) nerve-evoked mean increases in protein synthesis at a frequency of 10 Hz (142%) and 40 Hz (200%) were not affected in a statistically significant way (124 and 275%, respectively) by the neuronal type NO-synthase inhibitor N(w)propyl-l-arginine (N-PLA) (30 mg/kg intravenous). Neither were the increase (175%) in protein synthesis at 10 Hz in non-atropinized animals affected by N-PLA (180%). The increase (65%) in mitotic activity, 19 h after the end of stimulation at 40 Hz, in the presence of atropine, was not affected by N-PLA (55%). Neither were the increase (95%) in gland content of amylase at this point of observation statistically significant affected by N-PLA (144%). The secretion of fluid and output of amylase from the parotid gland upon nerve stimulation was not affected by N-PLA. When examining the non-selective NO-synthase inhibitor l-NAME (30 mg/kg intravenous) in atropinized rats subjected to stimulation at 10 Hz, neither the increase in protein synthesis nor the evoked fluid response or amylase outputs were affected. Hence, in contrast to an NO-dependent sympathetic-induced protein synthesis and mitosis in the parotid gland, involving the activity of the neuronal type NO-synthase, no support for a parasympathetic-induced protein synthesis (and gain in gland amylase) and mitosis, depending on NO-generation, was found. Likewise, the present findings provide no evidence for a role of NO in the parasym pathetic nerve-evoked fluid secretion and amylase output.
在戊巴比妥麻醉的大鼠中,于肾上腺素能受体阻断(酚妥拉明和普萘洛尔各2mg/kg静脉注射)状态下,分别在有无阿托品(2mg/kg静脉注射)以及有无一氧化氮合酶抑制剂的情况下,对耳颞副交感神经进行30分钟电刺激后,将放射性标记的亮氨酸和胸腺嘧啶掺入腮腺的三氯乙酸不溶性物质中,分别作为蛋白质合成和有丝分裂活性的指标。在阿托品化的大鼠中,副交感神经非肾上腺素能、非胆碱能(NANC)神经以10Hz(142%)和40Hz(200%)频率诱发的蛋白质合成平均增加,在统计学上未受到神经元型一氧化氮合酶抑制剂N(ω)-丙基-L-精氨酸(N-PLA)(30mg/kg静脉注射)的显著影响(分别为124%和275%)。非阿托品化动物在10Hz时蛋白质合成的增加(175%)也未受N-PLA(180%)的影响。在阿托品存在的情况下,40Hz刺激结束19小时后有丝分裂活性的增加(65%)未受N-PLA(55%)的影响。在该观察点腮腺淀粉酶含量的增加(95%)在统计学上也未受N-PLA(144%)的显著影响。神经刺激时腮腺的液体分泌和淀粉酶排出不受N-PLA的影响。当在10Hz刺激的阿托品化大鼠中检测非选择性一氧化氮合酶抑制剂L-NAME(30mg/kg静脉注射)时,蛋白质合成的增加、诱发的液体反应或淀粉酶排出均未受影响。因此,与腮腺中依赖一氧化氮的交感神经诱导的蛋白质合成和有丝分裂不同,后者涉及神经元型一氧化氮合酶的活性,未发现支持依赖一氧化氮生成的副交感神经诱导的蛋白质合成(以及腮腺淀粉酶增加)和有丝分裂的证据。同样,目前的研究结果也没有为一氧化氮在副交感神经诱发的液体分泌和淀粉酶排出中的作用提供证据。