Pipili E, Poyser N L
Prostaglandins. 1982 Mar;23(3):299-309. doi: 10.1016/0090-6980(82)90075-2.
Sympathetic nerve stimulation of the perfused mesenteric arterial bed of the rabbit, in vitro, increases the secretion of prostaglandin (PG)I2 and PGE2. Prazosin (4.8 X 10(-6) M), an alpha 1 adrenergic receptor antagonist, inhibited this increase in release of PGI2 but not of PGE2 whereas rauwolsin (10(-7) M), and alpha 2 adrenergic receptor antagonist, inhibited the increase in release of PGE2 but not PGI2. Prazosin (10(-6) M) completely blocked the vasoconstrictor response to nerve stimulation, and to norepinephrine and phenylephrine administration, suggesting there to be little of an alpha 2 adrenergic receptor component in this response. It is concluded that the increase in PGI2 release allows the activation of alpha1 adrenergic receptors and is therefore post-junctional in origin, whereas the increase in PGE2 release following the activation of alpha 2 adrenergic receptors and may be pre- and/or post-junctional in origin.
在体外对兔灌注肠系膜动脉床进行交感神经刺激,可增加前列腺素(PG)I2和PGE2的分泌。哌唑嗪(4.8×10⁻⁶ M),一种α1肾上腺素能受体拮抗剂,抑制了PGI2释放的增加,但不抑制PGE2的释放;而萝芙木碱(10⁻⁷ M),一种α2肾上腺素能受体拮抗剂,抑制了PGE2释放的增加,但不抑制PGI2的释放。哌唑嗪(10⁻⁶ M)完全阻断了对神经刺激以及去甲肾上腺素和苯肾上腺素给药的血管收缩反应,表明该反应中几乎不存在α2肾上腺素能受体成分。得出的结论是,PGI2释放的增加允许α1肾上腺素能受体激活,因此起源于节后;而α2肾上腺素能受体激活后PGE2释放的增加,其起源可能是节前和/或节后。