在兔主肺动脉中，α2 -肾上腺素能受体阻断、钠泵抑制及4 -氨基吡啶可增强前列腺素F2α对[3H]去甲肾上腺素释放的抑制作用。

The inhibitory action of PGF2 alpha on release of [3H]noradrenaline enhanced by alpha 2-adrenoceptor blockade, sodium-pump inhibition and 4-aminopyridine in the main pulmonary artery of the rabbit.

作者信息

Török T L, Bunyevácz Z, Nguyen T T, Hadházy P, Magyar K, Vizi E S

出版信息

Neuropharmacology. 1984 Jan;23(1):37-41. doi: 10.1016/0028-3908(84)90214-4.

Abstract

Large concentrations of prostaglandin PGF2 alpha inhibited the stimulation (2 Hz) evoked release of [3H]noradrenaline from the isolated main pulmonary artery of the rabbit (the inhibition caused by 3 X 10(-5) M PGF2 alpha was 62%). Furthermore, PGF2 alpha inhibited the release evoked by stimulation when it was enhanced by different procedures. During blockade of presynaptic alpha 2-adrenoceptors by 3 X 10(-7) M yohimbine, which by itself enhanced the overflow of [3H]NA in response to stimulation, the inhibitory action of PGF2 alpha was more pronounced (78.2%). In tissue in which the Na+-pump was inhibited (K+-free treatment) where the overflow of 3H was markedly increased, PGF2 alpha exerted nearly equal inhibition of transmitter release to that observed in control experiments (64.3%). The inhibitory effect of PGF2 alpha on the stimulation-evoked release of [3H]NA was less pronounced (32.1%) in the presence of 10(-4) M 4-aminopyridine (a blocker of K+-channels).

摘要

高浓度的前列腺素PGF2α抑制了（2赫兹）刺激诱发的家兔离体主肺动脉中[3H]去甲肾上腺素的释放（3×10−5M PGF2α引起的抑制率为62%）。此外，当通过不同程序增强刺激诱发的释放时，PGF2α也会抑制这种释放。在用3×10−7M育亨宾阻断突触前α2肾上腺素能受体期间，育亨宾本身会增强[3H]去甲肾上腺素对刺激的溢出反应，此时PGF2α的抑制作用更为明显（78.2%）。在Na+泵被抑制（无钾处理）的组织中，3H的溢出显著增加，PGF2α对递质释放的抑制作用与对照实验中观察到的几乎相同（64.3%）。在存在10−4M 4-氨基吡啶（一种钾通道阻滞剂）的情况下，PGF2α对刺激诱发的[3H]去甲肾上腺素释放的抑制作用不太明显（32.1%）。