前列腺素E2增强大鼠肠系膜动脉中去甲肾上腺素作用的机制
Mechanism of noradrenaline potentiation by prostaglandin E2 in rat mesenteric artery.
作者信息
Adeagbo A S, Okpako D T
出版信息
Br J Pharmacol. 1980;71(1):75-81. doi: 10.1111/j.1476-5381.1980.tb10911.x.
Abstract
1 Effects of prostaglandins E2 and F2 alpha (PGE2 and PGF2 alpha) on vasoconstrictor responses to noradrenaline (NA) and methoxamine in isolated mesenteric arteries of the rat were investigated. 2 PGE2 and to a lesser extent PGF2 alpha potentiated vasoconstrictor responses to NA and methoxamine. 3 Prior treatment with reserpine increased, and bretylium reduced, the extent of potentiation significantly. 4 NA vasoconstriction persisted for 1 h after Ca2+ was removed from the perfusing Krebs solution. Prostaglandin-induced potentiation was absent in Ca2+-free Krebs, but increased proportionately with increase in external Ca2+ concentration. 5 Vasoconstriction induced by high potassium, was not potentiated by PGE2. 6 It is concluded the PGE2 potentiates NA vasoconstriction by facilitating Ca2+ influx.
摘要
1 研究了前列腺素E2和F2α（PGE2和PGF2α）对大鼠离体肠系膜动脉中去甲肾上腺素（NA）和甲氧明血管收缩反应的影响。2 PGE2以及程度较轻的PGF2α增强了对NA和甲氧明的血管收缩反应。3 事先用利血平处理会显著增加这种增强程度，而用溴苄铵处理则会降低这种增强程度。4 从灌注的克雷布斯溶液中去除Ca2+后，NA血管收缩持续1小时。在无Ca2+的克雷布斯溶液中不存在前列腺素诱导的增强作用，但随着细胞外Ca2+浓度的增加成比例增加。5 高钾诱导的血管收缩未被PGE2增强。6 得出结论，PGE2通过促进Ca2+内流增强NA血管收缩。
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