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[神经肽Y减少大鼠血管中α1-肾上腺素能受体的脱敏作用]

[Neuropeptide Y reduces desensitization of alpha 1-adrenoceptors in rat blood vessels].

作者信息

Dong E D, Cheng M Z, Han Q D

机构信息

Institute of Vascular Medicine, Third Hospital, Beijing Medical University.

出版信息

Sheng Li Xue Bao. 1994 Aug;46(4):355-60.

PMID:7973826
Abstract

Vasoconstrictive responses to norepinephrine (NE) in isolated rat aorta and renal artery were respectively taken to represent the biological responses mediated by alpha 1B and alpha 1A subtype adrenoceptor (AR). After blood vessels were incubated with 10 mumol/L NE for 2 h, alpha 1-AR mediated vasocontraction was desensitized significantly, alpha 1B-AR being more marked than alpha 1A-AR. In the presence of 0.5 mumol/L neuropeptide Y (NPY), desensitization of alpha 1B-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 reduction of intracellular Ca2+ release were involved in the mechanism for desensitization of alpha 1B-AR.

摘要

在分离的大鼠主动脉和肾动脉中,对去甲肾上腺素(NE)的血管收缩反应分别代表由α1B和α1A亚型肾上腺素能受体(AR)介导的生物学反应。血管用10 μmol/L NE孵育2小时后,α1-AR介导的血管收缩明显脱敏,α1B-AR比α1A-AR更明显。在存在0.5 μmol/L神经肽Y(NPY)的情况下,α1B-AR的脱敏明显减弱。在大鼠主动脉中,NE介导的收缩包括相性和紧张性成分。用NE孵育后,相性收缩期延长但幅度减小,而紧张性收缩未见变化。在存在NPY的情况下,NE预孵育引起的相性收缩变化消失。提示细胞内Ca2+释放的延迟和减少参与了α1B-AR脱敏的机制。

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