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首页> 外文期刊>Neuropeptides: An International Journal >Vascular neuropeptide Y Y1-receptors in the rat kidney: vasoconstrictor effects and expression of Y1-receptor mRNA.
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Vascular neuropeptide Y Y1-receptors in the rat kidney: vasoconstrictor effects and expression of Y1-receptor mRNA.

机译:大鼠肾脏中的血管神经肽Y Y1受体:血管收缩作用和Y1受体mRNA的表达。

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Neuropeptide Y (NPY) -receptor subtypes were studied in the rat kidney in vivo by systemic administration of NPY, the two agonists [Leu(31), Pro(34)]NPY (Y1-receptor agonist) and NPY (13-36) (Y2-receptor agonist), or the Y1-receptor antagonist BIBP 3226. Effects on mean arterial blood pressure (MAP) and renal arterial blood flow were recorded. The Y1-receptor agonist evoked a dose-dependent increase in MAP concomitantly with a reduction in renal blood flow. At the largest dose administered (1.42 pmol/g), the Y1-agonist [Leu(31), Pro(34)] NPY increased MAP by 20 +/- 6 mmHg and reduced the renal vascular conductance by more than 50%. The same dose of the Y2-agonist NPY (13-36) did not evoke any clear-cut effects on the renal blood flow or MAP. Furthermore, administration of the Y1-receptor antagonist BIBP 3226 reduced the NPY-induced renal vasoconstriction, but did not affect the response to angiotensin II or phenylephrine. The effects evoked by 0.71 pmol/g NPY were almost abolished by 3 mg/kg BIBP 3226. In situ hybridization histochemistry was used to study the expression of Y1-receptor mRNA in the developing rat kidney. The levels of Y1-receptor mRNA expression in the vascular smooth muscle of the rat kidney varied at different ages, with low levels at postnatal day 10 and high levels at 20 days and again low levels at 40 days. In summary, the present study show a maturation-specific expression pattern of NPY Y1-receptor mRNA as well as functional effects of vascular NPY receptors of the Y1-subtype in the rat kidney. Copyright 1999 Harcourt Publishers Ltd.
机译:通过系统性施用NPY在大鼠肾脏体内研究了神经肽Y(NPY)受体亚型,这两种激动剂[Leu(31),Pro(34)] NPY(Y1-受体激动剂)和NPY(13-36) (Y2受体激动剂)或Y1受体拮抗剂BIBP3226。记录对平均动脉血压(MAP)和肾动脉血流的影响。 Y1受体激动剂引起MAP剂量依赖性增加,同时肾血流量减少。在最大剂量(1.42 pmol / g)下,Y1激动剂[Leu(31),Pro(34)] NPY使MAP升高20 +/- 6 mmHg,并使肾血管电导降低50%以上。相同剂量的Y2-激动剂NPY(13-36)对肾脏血流或MAP没有明显影响。此外,Y1受体拮抗剂BIBP 3226的给药可减少NPY诱导的肾血管收缩,但不影响对血管紧张素II或去氧肾上腺素的反应。 3 mg / kg BIBP 3226几乎消除了0.71 pmol / g NPY引起的作用。使用原位杂交组织化学研究了Y1受体mRNA在发育中大鼠肾脏中的表达。在大鼠肾脏的血管平滑肌中,Y1受体mRNA的表达水平随年龄的变化而变化,出生后第10天为低水平,第20天为高水平,第40天又为低水平。总之,本研究显示了大鼠肾脏中NPY Y1受体mRNA的成熟特异性表达模式以及Y1亚型的血管NPY受体的功能作用。版权所有1999 Harcourt Publishers Ltd.

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