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ω-3脂肪酸(二十二碳六烯酸和二十碳五烯酸)对去甲肾上腺素诱导的收缩的影响。

Effect of omega-3 fatty acids, docosahexaenoic and eicosapentaenoic, on norepinephrine-induced contractions.

作者信息

Engler M B

机构信息

Department of Physiological Nursing, University of California, San Francisco 94143-0610.

出版信息

Can J Physiol Pharmacol. 1992 May;70(5):675-9. doi: 10.1139/y92-086.

DOI:10.1139/y92-086
PMID:1423009
Abstract

The relaxant responses of the rat thoracic aorta to omega-3 fatty acids, docosahexaenoic and eicosapentaenoic, on norepinephrine- and potassium-induced contractions were investigated. Relaxation was enhanced in vessels contracted with norepinephrine. Docosahexaenoic acid at concentrations as low as 1, 3, and 10 microM evoked significant relaxant responses (15, 23, 30%) in norepinephrine-contracted vessels as compared with responses (5, 9, 12%) in potassium-contracted vessels. Results for eicosapentaenoic acid under similar conditions were 3, 8, and 19% in norepinephrine-contracted vessels and 3, 3, and 8% in potassium-contracted vessels. Pretreatment with eicosapentaenoic (10 microM) or docosahexaenoic acids (1-10 microM) decreased the contractile response to physiologic concentrations of norepinephrine. In the presence of calcium-free medium, the omega-3 fatty acids (1-30 microM) significantly abolished sustained norepinephrine contractions but did not reduce the phasic contractions when incubated prior to norepinephrine contraction. Comparatively, the effects of docosahexaenoic acid were greater than eicosapentaenoic acid. These findings suggest that the relaxant effects of the omega-3 fatty acids are specific to the mode of contraction, i.e., alpha-adrenoceptor stimuli. This effect may be related to intracellular calcium mechanisms, since both fatty acids reversed norepinephrine-induced sustained contractions in the absence of extracellular calcium.

摘要

研究了大鼠胸主动脉对ω-3脂肪酸二十二碳六烯酸和二十碳五烯酸对去甲肾上腺素和钾诱导收缩的舒张反应。去甲肾上腺素收缩的血管舒张增强。与钾收缩血管中的反应(5%、9%、12%)相比,低至1、3和10微摩尔浓度的二十二碳六烯酸在去甲肾上腺素收缩的血管中引起显著的舒张反应(15%、23%、30%)。在类似条件下,二十碳五烯酸在去甲肾上腺素收缩血管中的结果分别为3%、8%和19%,在钾收缩血管中的结果分别为3%、3%和8%。用二十碳五烯酸(10微摩尔)或二十二碳六烯酸(1 - 10微摩尔)预处理可降低对生理浓度去甲肾上腺素的收缩反应。在无钙培养基中,ω-3脂肪酸(1 - 30微摩尔)显著消除了去甲肾上腺素的持续收缩,但在去甲肾上腺素收缩前孵育时并未降低相位收缩。相比之下,二十二碳六烯酸的作用大于二十碳五烯酸。这些发现表明,ω-3脂肪酸的舒张作用对收缩模式具有特异性,即α-肾上腺素能受体刺激。这种作用可能与细胞内钙机制有关,因为在没有细胞外钙的情况下,两种脂肪酸都能逆转去甲肾上腺素诱导的持续收缩。

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