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
复制标题
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
中科院分区:
文献类型:
--
作者:
K. Malik;P. Ryan;J. Mcgiff
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.