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0-10006 The defect of translocation of AQP5 in parotid glands of streptozotocin-induced diabetic rats

Zhenfang Yuan ; Noriko Inoue ; Hirokazu lida ; Yasuko Ishikawa

Journal of Pharmacological Sciences, 2004, Vol.94 (suppl.1), p.75-75 [Periódico revisado por pares]

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Título:
0-10006 The defect of translocation of AQP5 in parotid glands of streptozotocin-induced diabetic rats
Autor: Zhenfang Yuan ; Noriko Inoue ; Hirokazu lida ; Yasuko Ishikawa
É parte de: Journal of Pharmacological Sciences, 2004, Vol.94 (suppl.1), p.75-75
Descrição: Parotid secretory response to acetyicholine (ACh) is reduced in streptozotocin-diabetic (STZ) rats. Here, we investigated the mechanisms involved in the decreased secretory response in coupled with the alteration of the distribution of aquaporin-5 (AQP5). Parotid slices from Wistar rats given STZ were incubated with or without M3-muscarinic ACh receptor (mAChR) agonists or other agents. Cevimeline hydrochloride (SNI-2011) increased AQP5 levels in apical plasma membrane (APM) by 3-fold in parotid glands in normal rats, but by 0. 8-fold in those of STZ rats. SNI-2011 increased AQP5 levels in basolateral membrane in STZ rats. Although mRNA levels for AQP5 were increased, the amount of AQP5 in parotid homogenate or lipid rafts was decreased in STZ rats. Both the quantities and affinity of mAChRs were decreased, but the amount of Gq protein was not changed in STZ rats in comparison with control rats. In conclusion, mACh agonists did not induce the increase in the amount of AQP5 in the APM of parotid glands from STZ rats because of the defect of translocation of AQP5 from rafts to the APM.
Editor: The Japanese Pharmacological Society
Idioma: Japonês

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