Modification by Prostaglandins E1 and E2Indomethacins, and Arachidonic Acid of the Vasoconstrictor Responses of the Isolated Perfused Rabbit and Rat Mesenteric Arteries to Adrenergic Stimuli

Modification by Prostaglandins E1 and E2Indomethacins, and Arachidonic Acid of the Vasoconstrictor Responses of the Isolated Perfused Rabbit and Rat Mesenteric Arteries to Adrenergic Stimuli
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前列腺素 E1 和 E2 吲哚美辛以及花生四烯酸对离体灌注兔和大鼠肠系膜动脉对肾上腺素刺激的血管收缩反应的调节

DOI:
10.1161/01.res.39.2.163
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发表时间:
1976
影响因子:
20.1
通讯作者:
J. Mcgiff
J. Mcgiff
中科院分区:
医学1区
文献类型:
--
作者:
K. Malik;P. Ryan;J. Mcgiff

文献摘要

被引文献

相似文献

在离体家兔肠系膜动脉灌注中,1-5 ng/ml的亲taglandin (PG) E1和E2没有改变基础灌注压,但降低了交感神经刺激时血管收缩的反应;受PGE2影响,PGE1和TariaMy对注射肾上腺素的反应降低。相比之下,在大鼠肠系膜动脉中,1-5 ng/ml的PGE1和PGE2可增强血管收缩剂对神经刺激和注射去甲肾上腺素的反应。在家兔肠系膜动脉中,PG合成抑制剂吲哚美辛增强了对交感神经刺激和注射去甲肾上腺素的反应,而在大鼠肠系膜动脉中,吲哚美辛抑制了对两种肾上腺素能刺激的反应。花生四烯酸,PG前体,在家兔对交感神经刺激和注射去甲肾上腺素的血管收缩反应降低,而在大鼠对肾上腺素能刺激的反应增强。由于花生四烯酸的这些作用通过同时输注吲哚美辛而被消除,它们似乎是通过花生四烯酸转化为PG介导的。我们得出结论,前列腺素调节肾上腺素能在肠系膜动脉中的传递,这种作用是物种依赖的。
In isolated perfused rabbit mesenteric arteries, pros-taglandin (PG) E1 and E2, 1-5 ng/ml, did not alter the basal perfasion pressure, but reduced tbe vasoconstrictor responses to sympathetic nerve stimulation; the responses to injected Borepinephrine were reduced by PGE1 and TariaMy affected by PGE2. In contrast, in rat mesenteric arteries PGE1 and PGE2, 1-5 ng/ml, potentiated the vasoconstrictor responses to nerve stimulation and to injected norepinephrine. In rabbit mesenteric arteries, tbe inhibitor of PG syatbesis, indometfaadn, augmented the responses to sympathetic nerve stimulation and to injected norepinephrine, whereas in rat mesenteric arteries indomethacin inhibited tbe responses to both adrenergic stimuli. Arachidonic acid, a PG precursor, reduced tbe vasoconstrictor responses to sympathetic nerve stimulation and to injected norepinephrine in rabbit, whereas in rat, potentiation of tbe responses to adrenergic stimuli occurred. Since these effects of arachidonic acid were abolished by tbe simultaneous infusion of indometfaacin, they appear to be mediated through conversion of arachidonic acid to PG. We conclude that prostaglandins modulate adrenergic transmission ia mesenteric arteries and this effect is species dependent.