THE INFLUENCE OF PROSTAGLANDINS ON NORADRENALINE‐INDUCED VASOCONSTRICTION IN ISOLATED PERFUSED MESENTERIC BLOOD VESSELS OF THE RAT
THE INFLUENCE OF PROSTAGLANDINS ON NORADRENALINE‐INDUCED VASOCONSTRICTION IN ISOLATED PERFUSED MESENTERIC BLOOD VESSELS OF THE RAT
复制标题
前列腺素对去甲肾上腺素诱导的大鼠离体肠系膜血管收缩的影响
DOI：
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发表时间：
1978
影响因子：
7.3
通讯作者：
P. McLennan
中科院分区：
文献类型：
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作者：
I. M. Coupar;P. McLennan
1研究吲哚美辛抑制去甲肾上腺素对大鼠肠系膜血管收缩反应及前列腺素E_2(PGE_2)和前列腺素E_1对其部分恢复作用。进一步的提示，前列腺素可能是去甲肾上腺素与该组织中的α-肾上腺素受体结合所必需的。2已报道的吲哚美辛的抑制作用得到证实，并进一步表明，去甲肾上腺素的量效曲线呈浓度依赖性的平坦化。3所有受试前列腺素均有浓度依赖性的修复作用。使吲哚美辛抑制的去甲肾上腺素反应恢复正常的效力由大到小依次为：前列腺素E_2、前列腺素E_1、前列环素A_1、前列环素_2、α、前列环素A_2。4所研究的前列腺素的修复作用并不一致，可分为两组。前列腺素E_2和前列腺素E_1恢复了对对照水平的反应，而前列腺素A_1、前列腺素A_2和前列腺素F_2α增加了对高于对照水平的反应，并且在较小的浓度范围内这样做。讨论了几种前列腺素受体的可能性。在恢复对对照水平PGA1的抑制反应方面，5个浓度的作用相当，但不能使PGE2恢复，使去甲肾上腺素的量效曲线平行左移，使基础灌流压小幅逐渐升高。6不同作用的原因尚不清楚，但似乎与酚妥拉明的PA2所指示的α肾上腺素受体的变化无关。此外，PGA1的恢复和增强作用不是通过阻断神经元对去甲肾上腺素的摄取来实现的。7去甲肾上腺素对大鼠肠系膜血管的收缩作用似乎需要前列腺素，而且这种作用是药物-受体相互作用的远端。讨论了前列腺素与细胞内钙离子的可能关系。
1 The report of the depression by indomethacin of vasoconstrictor responses to noradrenaline and their partial restoration by prostaglandin E2 (PGE2) and PGE1 in rat isolated perfused mesenteric blood vessels was investigated. The further suggestion that prostaglandins may be necessary for the combination of noradrenaline with the α‐adrenoceptor in this tissue was also studied. 2 The reported depression by indomethacin was confirmed and was further shown to be in the form of a concentration‐dependent flattening of the noradrenaline concentration‐effect curve. 3 A concentration‐dependent restorative effect was observed for all prostaglandins studied. The decreasing order of potency for the restoration towards normal of the indomethacin‐depressed responses to noradrenaline was: PGE2, PGE1, PGA1, PGF2α, PGA2. 4 The prostaglandins studied were not uniform in their restorative actions and could be separated into two groups. PGE2 and PGE1 restored responses towards the control level whereas PGA1, PGA2 and PGF2α increased responses to an above control level and did so over a smaller concentration range. The possibility of several prostaglandin receptors is discussed. 5 At concentrations equi‐effective in restoring depressed responses to control levels PGA1 but not PGE2, caused a parallel shift of the noradrenaline concentration‐effect curve to the left and a small, gradual rise in the basal perfusion pressure. 6 The reason for the differing effects remains obscure but does not seem to involve a change in the α‐adrenoceptor as indicated by the pA2 of phentolamine. Furthermore, the restorative and potentiating effect of PGA1 is not mediated by blockade of neuronal uptake of noradrenaline. 7 It appears that prostaglandins are required for the vasoconstrictor action of noradrenaline in rat mesenteric blood vessels and that this effect is distal to the drug‐receptor interaction. The possible involvement of prostaglandins with intracellular calcium ions is discussed.