Engler M B
Department of Physiological Nursing, University of California, San Francisco 94143-0610.
Cardiovasc Drugs Ther. 1992 Dec;6(6):605-10. doi: 10.1007/BF00052562.
The vasorelaxant activity of the omega-3 fatty acids--docosahexaenoic (DHA) and eicosapentaenoic (EPA) acids--in comparison with other known vasodilators--sodium nitroprusside, nitroglycerin, papaverine, and D600--were studied in the isolated rat aorta. The relaxant responses of these vasodilators and fatty acids at concentrations of 1-100 microM were assessed in aortic rings contracted with norepinephrine (NE 10(-6) M) or with KCl (30 mM). Cyclic nucleotide enhancers (sodium nitroprusside, nitroglycerin, papaverine) were more effective in producing relaxation, regardless of the contractile mechanism, i.e., alpha-adrenoceptor stimulation or depolarization. In contrast, the omega-3 fatty acids produced augmented relaxation in NE-contracted vessels. Relaxations produced by DHA (15 +/- 2% to 45 +/- 10%) were similar to D600 (16 +/- 2% to 60 +/- 7%) in NE-contracted rings, but not in KCl contracted rings. The responses to D600 and DHA in KCl-contracted vessels were 79 +/- 2% to 104 +/- 3% and 5 +/- 1% to 21 +/- 3%, respectively. In another set of experiments, the effects of omega-3 fatty acids in the presence of albumin were examined; no significant differences in the induced relaxant responses were noted. These results suggest that the mechanisms of vascular relaxation, such as cyclic nucleotide elevation and calcium antagonism of potential-operated channels, are different from those induced by the omega-3 fatty acids.
在离体大鼠主动脉中，研究了ω-3脂肪酸（二十二碳六烯酸（DHA）和二十碳五烯酸（EPA））与其他已知血管舒张剂（硝普钠、硝酸甘油、罂粟碱和D600）相比的血管舒张活性。在与去甲肾上腺素（NE 10⁻⁶ M）或氯化钾（30 mM）收缩的主动脉环中，评估了这些血管舒张剂和脂肪酸在1-100 μM浓度下的舒张反应。环核苷酸增强剂（硝普钠、硝酸甘油、罂粟碱）在产生舒张方面更有效，无论收缩机制如何，即α-肾上腺素能受体刺激或去极化。相比之下，ω-3脂肪酸在NE收缩的血管中产生增强的舒张作用。在NE收缩的环中，DHA产生的舒张作用（15±2%至45±10%）与D600（16±2%至60±7%）相似，但在KCl收缩的环中则不同。在KCl收缩的血管中，对D600和DHA的反应分别为79±2%至104±3%和5±1%至21±3%。在另一组实验中，研究了ω-3脂肪酸在白蛋白存在下的作用；未观察到诱导的舒张反应有显著差异。这些结果表明，血管舒张机制，如环核苷酸升高和潜在操作通道的钙拮抗作用，与ω-3脂肪酸诱导的机制不同。
