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肾上腺素能刺激对人体尿前列腺素E2和6-酮前列环素F1α的影响。

The effect of adrenergic stimulation on urinary prostaglandin E2 and 6 keto PGF1 alpha in man.

作者信息

Nadler J, Zipser R D, Horton R

出版信息

Prostaglandins. 1983 Oct;26(4):519-30. doi: 10.1016/0090-6980(83)90190-9.

Abstract

To evaluate the details of the adrenergic stimulation of urinary prostaglandins in man, ten normal volunteers were given various agonists and antagonists. The effect of 4 hour IV infusions of norepinephrine (NE), NE + phentolamine (PHT), NE + phenoxybenzamine (PHB), NE + prazosin (PZ), isoproterenol (ISO), and PHT alone on urinary PGE2 and PGI2 (6 keto PGF1 alpha) were determined. PGE2 and 6 keto PGF1 alpha were measured by radioimmunoassay from 4 hour urine samples. NE stimulated both PGE2 (196 +/- 40 to 370 +/- 84 ng/4 hrs/g creatinine and 6 keto PGF1 alpha (184 +/- 30 to 326 +/- 36), both p less than 0.01. In contrast, ISO had no effect on either PGE2 or 6 keto PGF1 alpha excretion. Alpha blockade with PHT. PHB, or PZ inhibited the NE induced systemic pressor effect. However, the effect of the alpha blockers on the NE induced stimulation of PGE2 and 6 keto PGF1 alpha varied. PHT did not alter the NE stimulated PGE2 or 6 keto PGF1 alpha release (370 +/- 84 vs. 381 +/- 80) PGE2 and (326 +/- 50 vs. 315 +/- 40) 6 keto PGF1 alpha both p greater than 0.2). PHT alone stimulated only 6 keto PGF1 alpha. PHB and the specific alpha 1 antagonist PZ similarly eliminated the NE induced prostaglandin release. These results suggest that adrenergically mediated urinary prostaglandin release in man is via an alpha receptor with alpha 1 characteristics.

摘要

为评估人体中肾上腺素能刺激尿前列腺素的具体情况,对10名正常志愿者给予了各种激动剂和拮抗剂。测定了静脉输注去甲肾上腺素(NE)、NE + 酚妥拉明(PHT)、NE + 酚苄明(PHB)、NE + 哌唑嗪(PZ)、异丙肾上腺素(ISO)以及单独使用PHT 4小时对尿PGE2和PGI2(6-酮-PGF1α)的影响。通过放射免疫分析法测定4小时尿液样本中的PGE2和6-酮-PGF1α。NE刺激了PGE2(从196±40至370±84 ng/4小时/克肌酐)和6-酮-PGF1α(从184±30至326±36),两者p均小于0.01。相比之下,ISO对PGE2或6-酮-PGF1α排泄均无影响。用PHT、PHB或PZ进行α阻断可抑制NE诱导的全身升压作用。然而,α受体阻滞剂对NE诱导的PGE2和6-酮-PGF1α刺激的影响各不相同。PHT未改变NE刺激的PGE2或6-酮-PGF1α释放(PGE2为370±84对381±80,6-酮-PGF1α为326±50对315±40,两者p均大于0.2)。单独使用PHT仅刺激6-酮-PGF1α。PHB和特异性α1拮抗剂PZ同样消除了NE诱导的前列腺素释放。这些结果表明,人体中肾上腺素能介导的尿前列腺素释放是通过具有α1特性的α受体实现的。

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