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血管紧张素II诱导兔脾包膜条收缩及前列腺素释放。使用前列腺素E1和E2的放射免疫测定法。

Angiotensin II-induced contractions of rabbit splenic capsular strips and release of prostaglandins. Use of radioimmunoassays for prostaglandins E1 and E2.

作者信息

Diekmann J M, Jobke A, Peskar B A, Hertting G

出版信息

Naunyn Schmiedebergs Arch Pharmacol. 1977 Mar;297(2):177-83. doi: 10.1007/BF00499928.

Abstract

Rabbit splenic capsular strips contract in response to angiotensin II and simultaneously release prostaglandins E and F into the bath fluid. Contractions, though not sustained, and prostaglandin release are dependent on the concentrations of angiotensin II. Addition of indometacin to the bath fluid inhibits prostaglandin release and potentiates the angiotensin II-induced contractions. Similarly, 5,8,11,14-eicosatetraynoic acid, another blocker of prostaglandin synthesis, potentiates contractions elicited by angiotensin II. Exogenous prostaglandin E1 (300 ng/ml) tends to decrease angiotensin II-induced contractions, while prostaglandin E2 (300 ng/ml) as well as prostaglandin F2alpha (300 ng/ml) significantly increase the contractions produced by angiotensin II. The prostaglandin endoperoxide analogues (15S)-hydroxy-9alpha,11alpha-(epoxymethano)prosta-5Z,13 E-dienoic acid and (15S)-hydroxy-11alpha,9alpha-(epoxymethano)-prosta-5Z,13 E-dienoic acid in concentrations of 300 ng/ml are either without effect or weak smooth muscle stimulants of their own, but do not influence the effect of angiotensin II. By the simultaneous use of sensitive and specific radioimmunoassays for prostaglandins E1 and E2 the prostaglandin E-like substance released by the rabbit splenic capsular strips was found to resemble serologically much more the dienoic prostaglandin E2 than prostaglandin E1. The potentation of the effect of angiotensin II by indometacin and 5,8,11,14-eicosatetraynoic acid might be caused by inhibition of synthesis of prostaglandins or related compounds in the splenic tissue. However, an undefined sensitizing effect of indometacin and 5,8,11,14-eicosatetraynoic acid, not related to their effect on prostaglandin synthetase, on the smooth muscle preparation cannot be excluded.

摘要

兔脾包膜条对血管紧张素II产生收缩反应,并同时向浴液中释放前列腺素E和F。收缩反应虽不持久,但前列腺素释放量取决于血管紧张素II的浓度。向浴液中添加吲哚美辛可抑制前列腺素释放,并增强血管紧张素II诱导的收缩。同样,另一种前列腺素合成阻滞剂5,8,11,14-二十碳四烯酸也能增强血管紧张素II引起的收缩。外源性前列腺素E1(300 ng/ml)倾向于减少血管紧张素II诱导的收缩,而前列腺素E2(300 ng/ml)以及前列腺素F2α(300 ng/ml)则显著增强血管紧张素II产生的收缩。浓度为300 ng/ml的前列腺素内过氧化物类似物(15S)-羟基-9α,11α-(环氧亚甲基)前列腺-5Z,13 E-二烯酸和(15S)-羟基-11α,9α-(环氧亚甲基)-前列腺-5Z,13 E-二烯酸要么没有作用,要么自身就是弱平滑肌刺激剂,但不影响血管紧张素II的作用。通过同时使用针对前列腺素E1和E2的灵敏且特异的放射免疫分析法,发现兔脾包膜条释放的类前列腺素E物质在血清学上与二烯酸前列腺素E2的相似性远高于前列腺素E1。吲哚美辛和5,8,11,14-二十碳四烯酸对血管紧张素II作用的增强可能是由于抑制了脾组织中前列腺素或相关化合物的合成。然而,不能排除吲哚美辛和5,8,11,14-二十碳四烯酸对平滑肌制剂有未明确的致敏作用,且这种作用与其对前列腺素合成酶的作用无关。

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