Nakajima M, Toda N
Prostaglandins. 1984 Mar;27(3):407-19. doi: 10.1016/0090-6980(84)90199-0.
Treatment with prostaglandin (PG) D2 in concentrations (10(-8) to 10(-7) M) insufficient to alter the basal tone potentiated the contractile response of helical strips of dog mesenteric arteries to transmural electrical stimulation but did not influence the response to norepinephrine. The potentiating effect of PGD2 was not prevented by treatment with diphloretin phosphate, a PG antagonist, whereas contractions of dog cerebral arteries induced by PGD2 were suppressed. The 3H-overflow evoked by transmural stimulation in superfused mesenteric arterial strips previously soaked in 3H-norepinephrine containing media was significantly increased in PGD2. It is concluded that PGD2 increases the stimulation-evoked release of norepinephrine from adrenergic nerves innervating the arterial wall. PGD2 appears to act differently on receptive sites responsible for increasing the release of norepinephrine and for producing arterial contraction.
用浓度为10⁻⁸至10⁻⁷M的前列腺素（PG）D₂进行处理，该浓度不足以改变基础张力，但能增强犬肠系膜动脉螺旋条对跨壁电刺激的收缩反应，而对去甲肾上腺素的反应没有影响。PG拮抗剂磷酸二氢杨梅素处理并不能阻止PGD₂的增强作用，而PGD₂诱导的犬脑动脉收缩则受到抑制。预先浸泡在含³H-去甲肾上腺素培养基中的灌注肠系膜动脉条经跨壁刺激诱发的³H溢出在PGD₂作用下显著增加。得出的结论是，PGD₂增加了去甲肾上腺素能神经向动脉壁释放刺激诱发的去甲肾上腺素。PGD₂似乎对负责增加去甲肾上腺素释放和引起动脉收缩的受体部位有不同的作用。
