首页> 外文期刊>Vascular pharmacology >Marked neuropeptide Y-induced contractions via NPY-Y1 receptor and its desensitization in rat veins.
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Marked neuropeptide Y-induced contractions via NPY-Y1 receptor and its desensitization in rat veins.

机译:明显的神经肽Y通过NPY-Y1受体引起的收缩及其在大鼠静脉中的脱敏作用。

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The aim of this study was to investigate neuropeptide Y (NPY)-induced vasoconstrictions in rat blood vessels and which NPY receptor subtype is involved in vasoconstrictions. NPY produced marked contractions in rat common jugular, brachial, portal, femoral and tail veins, and vena cava inferior, whereas it produced little or no contractions in rat common carotid, brachial, femoral and tail arteries, and thoracic and abdominal aortae. The maximal NPY-induced contractions were larger than maximal phenylephrine (PE)-induced contractions in the veins. These NPY-induced contractions were blocked by the Y1 antagonists, SRL-21, and BIBP3226 but not by the Y5 antagonist, L-152804. A Y2 agonist, NPY (13-36), did not produce contractions. RT-PCR showed that NPY-Y1 was the only receptor subtype in the veins indicating that NPY-induced contractions are mediated through the Y1 receptor. Pretreatment with NPY showed a rapid and long-lasting desensitization of these contractions. The marked NPY-induced contractions and its desensitization in the veins suggest the physiological relevance of NPY in the venous circulation.
机译:这项研究的目的是调查大鼠血管中神经肽Y(NPY)诱导的血管收缩以及该血管收缩涉及哪些NPY受体亚型。 NPY在大鼠的普通颈,臂,门,股​​和尾静脉以及下腔静脉中产生明显的收缩,而在大鼠的颈总动脉,臂,股,尾动脉,胸和腹主动脉中几乎没有或没有收缩。 NPY引起的最大收缩大于最大苯肾上腺素(PE)引起的静脉收缩。这些NPY诱导的收缩被Y1拮抗剂SRL-21和BIBP3226阻断,但未被Y5拮抗剂L-152804阻断。 Y2激动剂NPY(13-36)不会产生收缩。 RT-PCR显示,NPY-Y1是静脉中唯一的受体亚型,表明NPY诱导的收缩是通过Y1受体介导的。 NPY预处理显示这些收缩迅速而持久地脱敏。 NPY引起的明显收缩及其在静脉中的脱敏性提示NPY在静脉循环中的生理相关性。

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