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PP56(D-肌醇1,2,6-三磷酸)对神经肽Y诱导的去甲肾上腺素诱导的血管收缩增强作用的抑制。

Inhibition of neuropeptide Y-induced potentiation of noradrenaline-induced vasoconstriction by PP56 (D-myo-inositol 1,2,6-tris-phosphate).

作者信息

Adamsson M, Fallgren B, Edvinsson L

机构信息

Department of Experimental Research, Malmö General Hospital, Sweden.

出版信息

Br J Pharmacol. 1992 Jan;105(1):93-6. doi: 10.1111/j.1476-5381.1992.tb14216.x.

Abstract
  1. Although neuropeptide Y (NPY) is a potent vasoconstrictor in many vascular beds, nanomolar concentrations of this peptide potentiate the noradrenaline-induced contractions in rabbit gastroepiploic and femoral arteries, and guinea-pig mesenteric and uterine arteries. 2. The potentiating effect of NPY on noradrenaline-induced contraction was present in endothelium-denuded femoral arteries. 3. The potentiating effect of NPY on noradrenaline-induced contraction was antagonized by PP56 (D-myo-inositol 1,2,6-trisphosphate) in low concentrations (down to 0.1 nM). This antagonistic effect was observed in all four types of vessels studied. Contractions induced by noradrenaline, histamine, endothelin-1 and potassium were not altered by PP56 in concentrations upto 1 microM in femoral artery of rabbit. 4. We provide evidence that a non-peptide (PP56) can selectively antagonize NPY-induced effects in rabbit and guinea-pig peripheral arteries without affecting the vasoconstrictor response to noradrenaline.
摘要
  1. 尽管神经肽Y(NPY)在许多血管床中是一种强效血管收缩剂,但纳摩尔浓度的这种肽可增强去甲肾上腺素诱导的兔胃网膜动脉和股动脉以及豚鼠肠系膜动脉和子宫动脉的收缩。2. NPY对去甲肾上腺素诱导的收缩的增强作用在去内皮的股动脉中存在。3. NPY对去甲肾上腺素诱导的收缩的增强作用在低浓度(低至0.1 nM)时被PP56(D-肌醇1,2,6-三磷酸)拮抗。在所有四种研究的血管类型中均观察到这种拮抗作用。在兔股动脉中,浓度高达1 microM的PP56不会改变去甲肾上腺素、组胺、内皮素-1和钾诱导的收缩。4. 我们提供的证据表明,一种非肽(PP56)可以选择性拮抗兔和豚鼠外周动脉中NPY诱导的效应,而不影响对去甲肾上腺素的血管收缩反应。

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