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首页> 外文期刊>Prostaglandins, Leukotrienes, and Essential Fatty Acids >Bradykinin and electrical stimulation increase prostaglandin production in the rat vas deferens.
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Bradykinin and electrical stimulation increase prostaglandin production in the rat vas deferens.

机译:缓激肽和电刺激可增加大鼠输精管中前列腺素的产生。

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摘要

The epididymal portion of the rat vas deferens produced prostaglandins (PG) E(2), F(2alpha)and 6-keto F(1alpha). Electrical stimulation (ES, 0.1 Hz, 1 ms) increased such production by 100%, and similar results were obtained in the presence of 1.0 microM bradykinin (Bk). When both stimuli were applied simultaneously, the increases in PG production were 1100% for PGE(2), 800% for PGF(2alpha)and 400% for PG6-keto F(1alpha). Prazosin abolished the effect of ES on PG production. A selective Bk B(2)-receptor antagonist abolished the increase in PG production induced by Bk, both in non-stimulated and in ES tissues. Bk (1.0 microM) elicited contractile responses in non-stimulated as well as in ES tissues, responses that were not modified in the presence of 10 microM indomethacin. In conclusion, the effects of Bk on prostaglandin production appears to depend on the activation of B(2) receptors, while the increase in prostaglandin release induced by ES, and the effects observed with both stimuli simultaneously, should be mediated by the release of noradrenaline and the subsequent activation of alpha(1) adrenoceptors. Copyright 2001 Harcourt Publishers Ltd.
机译:大鼠输精管的附睾部分产生前列腺素(PG)E(2),F(2alpha)和6-酮F(1alpha)。电刺激(ES,0.1 Hz,1 ms)使这种产生增加了100%,并且在存在1.0 microM缓激肽(Bk)的情况下获得了相似的结果。当同时应用两种刺激时,PG的增加对于PGE(2)为1100%,对于PGF(2alpha)为800%,对于PG6-酮F(1alpha)为400%。哌唑嗪消除了ES对PG生产的影响。选择性的Bk B(2)受体拮抗剂消除了在非刺激和ES组织中Bk诱导的PG产生的增加。 Bk(1.0 microM)在未刺激的以及在ES组织中引起收缩反应,在10 microM消炎痛存在下其反应没有改变。总之,Bk对前列腺素产生的影响似乎取决于B(2)受体的激活,而ES诱导的前列腺素释放的增加以及两种刺激同时观察到的影响,应该通过去甲肾上腺素的释放来介导。以及随后激活的alpha(1)肾上腺素受体。版权所有2001 Harcourt Publishers Ltd.。

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