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神经肽Y可减轻大鼠血管α1肾上腺素受体亚型的脱敏作用

^NEUROPEPTIDE Y REDUCES DESENSITIZATION OF α1-ADRENOCEPTORS IN RAT BLOOD VESSELS

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【作者】 董尔丹陈明哲韩启德

【Author】 DONG ER-DAN; CHENG MING-ZHE AND HAN QI-DE (CHIDE HAN)(Institute of Vascular Medicine, The Third Hospital, Beijing Medical University, Beijing 100083)

【机构】 北京医科大学第三医院血管医学研究所

【摘要】 以离体大鼠主动脉与肾动脉对去甲肾上腺素(NE)的收缩反应分别代表α1B与α1A亚型肾上腺素受体(AR)激动时的生物学效应。血管经NE10μmol/L温育2h后,α1-AR介导收缩效应的敏感性显著降低,其中α1B亚型AR的脱敏程度显著大于α1A亚型AR。上述经NE温育的血管,在神经肽Y(NPY)0.5μmol/L存在时,α1B亚型AR的脱敏程度显著减轻。NE收缩主动脉的两时相分析表明,脱敏时主要表现为相性收缩时间延长,收缩幅度降低,而紧张性收缩并无显著改变;在NPY存在时上述相性收缩改变消失。提示α1B亚型AR脱敏的机制主要与细胞内Ca2+动员减慢减少有关。

【Abstract】 Vasoconstrictive responses to norepinephrine (NE) in isolated rat aorta and renal artery were respectively taken to represent the biological responses mediated by α1B and α1A subtype adrenoceptor (AR). After blood vessels were incubated with 10 μmol/L NE for 2 h, α1-AR mediated vasocontraction was desensitized significantly, α1B-AR being more marked than α1-AR. In the presence of 0. 5 μmol/L neuropeptide Y (NPY), desensitization of α1B-AR was attenuated significantly. In rat aorta the NE-mediated contraction comprised both phasic and tonic elements. After the incubation with NE, the phasic contraction period was prolonged but magnitude decreased, while no change was found for the tonic contraction. In the presence of NPY, the changes of phasic contraction caused by NE preincubation disappeared. It is suggested that retardation and deduction of intracellular Ca2+ release were involved in the mechanism for desensitization of α1B-AR.

【基金】 国家自然科学基金
  • 【文献出处】 生理学报 ,ACTA PHYSIOLOGICA SINICA , 编辑部邮箱 ,1994年04期
  • 【分类号】R338
  • 【被引频次】11
  • 【下载频次】44
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