Mechanisms underlying neurotransmitter-regulation of the amount of aquaporin-5 in the apical plasma memnranes in rat parotid glands and age-dependent changes of it.

唾液腺是由自主神经产生的。刺激组织中的毒蕈碱和a-和B-肾上腺素能受体激活唾液分泌。水通道蛋白-5（Aquaporin-5）是从大鼠下颌下腺中克隆的一种蛋白质，定位于腮腺导管细胞的顶端质膜（APM）。为了探讨水通道蛋白-5在神经刺激诱导的唾液分泌中的作用，本研究采用免疫印迹法研究了乙酰胆碱和肾上腺素诱导的大鼠腮腺组织水通道蛋白-5分布的变化。乙酰胆碱或肾上腺素处理1 min内可引起APM中水通道蛋白-5含量增加，处理10 min以上则引起APM中水通道蛋白-5含量减少。阿托品、p-F-HHSiD和TMB-8可抑制乙酰胆碱引起的APM中水通道蛋白-5含量增加，而甲基辛四明、GF-109203 X和H-7则不能抑制乙酰胆碱引起的APM中水通道蛋白-5含量增加。A-23187单药 ...更多信息 肾上腺素诱导的APM中水通道蛋白-5含量的增加被苯肾上腺素模拟，而可乐定、多巴酚丁胺和沙丁胺醇则不能模拟。酚妥拉明可抑制此作用，普萘洛尔则无此作用。上述结果表明，乙酰胆碱和肾上腺素分别作用于M3-M受体和Al-肾上腺素能受体，引起APM中水通道蛋白-5含量的增加，而乙酰胆碱和肾上腺素引起的[Ca ~（2+）]i升高可能在这种增加中起关键作用。乙酰胆碱可使青年大鼠APM中水通道蛋白-5的含量增加3倍，而使老年大鼠APM中水通道蛋白-5的含量增加2倍。大鼠APM中水通道蛋白5含量的差异可能取决于乙酰胆碱升高[Ca ~（2+）]i的差异。少

Salivary glands are innovated by the autonomic nerve. The stimulations of muscarinic and a- and b- adrenergic receptors in the tissues activate the salivary secretion. Aquaporin-5 which was cloned from submandibular glands was shown to be localized topographically in the apical plasma membrane (APM) of duct cells in rat parotid glands. In this investigation, to evaluate the role of aquaporin-5 in salivary secretion induced by nervous stimulation, the alteration of the distribution of aquaporin-5 in rat parotid tissues induced by acetylcholine or epinephrine was studied by immunoblot analysis. The treatment of the tissues with acetylcholine or epinephrine within 1 min induced the increase in the amount of aquaporin-5 in APM, but that for more than 10 min resulted in the decrease of the amount of aquaporin-5 in APM.Acetylcholine-induced increase in the amount of aquaporin-5 in APM was inhibited by atropine, p-F-HHSiD and TMB-8, but not by methoctramine, GF-109203X or H-7. A-23187 alone s … More timulated the increase in the amount of aquaporin-5 in APM.While, epinephrine-induced increase in the amount of aquaporin-5 in APM was mimicked by phenylephrine, but not by clonidine, dobutamine, or salbutamol. It was inhibited by phentolamine, but not by propranolol. Furthermore, epinephrinethe-induced increase of aquaporin-5 was inhibited by cytochalasin-D and tubulozole-C.These results indicated that acetylcholine and epinephrine acted on M3-muscarinic and al-adrenergic receptors, respectively and induced the increase in the amount of aquaporin-5 in APM, and that [Ca2+]i elevation by acetylcholine or epinephrine may play a key role in this increase. In addition the involvement of the cytoskeleton was shown in these induction.The increase of the amount of aquaporin-5 in APM by acetylcholine was 3-fold in the tissues of young adult rats, but 2-fold in those of senescent rats. The difference between the amounts of aquaporin-5 in APM in these rats may depend on that between the [Ca2+]i elevated by acetylcholine. Less