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环磷酸腺苷不会抑制培养的兔肾微血管内皮细胞中由A23187诱导的前列腺素生物合成。

Cyclic AMP does not inhibit A23187-induced prostaglandin biosynthesis in cultured rabbit renal microvascular endothelial cells.

作者信息

Chaudhari A, Gupta S, Kirschenbaum M A

机构信息

Department of Medicine, University of California, Irvine.

出版信息

Prostaglandins Leukot Essent Fatty Acids. 1990 Oct;41(2):119-23. doi: 10.1016/0952-3278(90)90064-r.

DOI:10.1016/0952-3278(90)90064-r
PMID:1703311
Abstract

We have previously shown that cultured rabbit renal preglomerular microvascular endothelial cells have the ability to synthesize a number of common prostaglandins. In the present study we have examined whether endogenous cyclic AMP is involved in the regulation of PGI2 and PGE2 biosynthesis in these cultured cells. Isoproterenol and forskolin produced an increase in cyclic AMP accumulation in these cells but had no effect on PGI2 or PGE2 biosynthesis either in the presence or absence of A23187. Similar results were noted in the presence of 3-isobutyl-1-methylxanthine, a cyclic AMP-phosphodiesterase inhibitor. These studies suggested that endogenous cyclic AMP does not regulate the biosynthesis of PGI2 or PGE2 in cultured renal preglomerular microvascular endothelial cells either under basal or A23187-stimulated condition. They further suggested that the effect of 3-isobutyl-1-methylxanthine on prostaglandin biosynthesis in these cultured cells was not secondary to its effects on phosphodiesterase.

摘要

我们之前已经表明,培养的兔肾球前微血管内皮细胞具有合成多种常见前列腺素的能力。在本研究中,我们检测了内源性环磷酸腺苷(cAMP)是否参与这些培养细胞中前列环素(PGI2)和前列腺素E2(PGE2)生物合成的调节。异丙肾上腺素和福斯高林使这些细胞中的环磷酸腺苷积累增加,但在存在或不存在A23187的情况下,对PGI2或PGE2的生物合成均无影响。在存在环磷酸腺苷磷酸二酯酶抑制剂3-异丁基-1-甲基黄嘌呤的情况下也观察到了类似结果。这些研究表明,内源性环磷酸腺苷在基础条件下或A23187刺激条件下均不调节培养的肾球前微血管内皮细胞中PGI2或PGE2的生物合成。它们进一步表明,3-异丁基-1-甲基黄嘌呤对这些培养细胞中前列腺素生物合成的影响并非继发于其对磷酸二酯酶的作用。

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1
Cyclic AMP does not inhibit A23187-induced prostaglandin biosynthesis in cultured rabbit renal microvascular endothelial cells.环磷酸腺苷不会抑制培养的兔肾微血管内皮细胞中由A23187诱导的前列腺素生物合成。
Prostaglandins Leukot Essent Fatty Acids. 1990 Oct;41(2):119-23. doi: 10.1016/0952-3278(90)90064-r.
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