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巴特综合征由血管活性激素失衡引起。

Bartter's syndrome results from an imbalance of vasoactive hormones.

作者信息

McGiff J C

出版信息

Ann Intern Med. 1977 Sep;87(3):369-72. doi: 10.7326/0003-4819-87-3-369.

Abstract

Bartter's syndrome may result from a disturbance of the interrelations of three vasoactive hormonal systems: the kallikrein-kinin, renin-angiotensin, and prostaglandin systems. Although kinin and angiotensin have opposing effects on renal function, each hormone increases the levels of prostaglandins within the kidney. Elevated renal prostaglandin levels are primarily responsible for some of the major features of the syndrome. The effectiveness of indomethacin in the treatment of Bartter's syndrome derives in large part from the ability of the drug to inhibit prostaglandin production. Indomethacin also decreases the activity of the renin-angiotensin system and the excretion of renal kallikrein, perhaps related to inhibition of prostaglandin mechanisms that may participate in the release of renin and kallikrein. However, additional actions of indomethacin must be considered, such as an effect of the drug on a naturally occurring renin inhibitor.

摘要

巴特综合征可能源于三种血管活性激素系统(激肽释放酶 - 激肽系统、肾素 - 血管紧张素系统和前列腺素系统)相互关系的紊乱。尽管激肽和血管紧张素对肾功能有相反的作用,但每种激素都会增加肾脏内前列腺素的水平。肾脏前列腺素水平升高是该综合征一些主要特征的主要原因。吲哚美辛治疗巴特综合征的有效性在很大程度上源于该药物抑制前列腺素产生的能力。吲哚美辛还会降低肾素 - 血管紧张素系统的活性和肾脏激肽释放酶的排泄,这可能与抑制可能参与肾素和激肽释放酶释放的前列腺素机制有关。然而,必须考虑吲哚美辛的其他作用,例如该药物对天然存在的肾素抑制剂的影响。

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