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进行创新的。刺激组织中的M受体和a-和b-肾上腺素能受体可以激活唾液分泌。水通道蛋白-5是从颌下腺中克隆出来的，定位于大鼠腮腺导管细胞的顶端质膜。为探讨水通道蛋白-5在神经刺激诱导的唾液分泌中的作用，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中水通道蛋白-5分布的变化。用乙酰胆碱或肾上腺素处理APM 1min内可引起APM水通道蛋白-5含量增加，但处理10min以上可使APM水通道蛋白-5含量减少。阿托品、p-F-HHSiD和TMB-8可抑制乙酰胆碱诱导的APM水通道蛋白-5含量增加，而甲氧曲明、GF-109203X和H-7对此无影响。A-23187仅S一家…肾上腺素诱导的APM水通道蛋白-5的增加可被苯肾上腺素所模拟，但不能被可乐定、多巴酚丁胺或沙丁胺醇所模拟。它可被酚妥拉明抑制，但不能被心得安抑制。此外，肾上腺素诱导的水通道蛋白-5的增加可被细胞松弛素-D和管洛唑-C所抑制。这些结果表明，乙酰胆碱和肾上腺素分别作用于M_3-M受体和肾上腺素能受体，并诱导APM水通道蛋白-5的含量增加，而乙酰胆碱或肾上腺素引起的[Ca~(2+)]i升高可能在此过程中起关键作用。乙酰胆碱使幼年大鼠APM组织中水通道蛋白-5的含量增加3倍，而衰老大鼠则增加2倍。这些大鼠APM内水通道蛋白-5含量的差异可能取决于乙酰胆碱升高的[Ca~(2+)]i之间的差异。较少

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