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糖皮质激素诱导的高血压:从小鼠到人类

Glucocorticoid-induced hypertension: from mouse to man.

作者信息

Whitworth J A, Schyvens C G, Zhang Y, Mangos G J, Kelly J J

机构信息

The John Curtin School of Medical Research, The Australian National University, Acton, Australian Capital Territory, Australia.

出版信息

Clin Exp Pharmacol Physiol. 2001 Dec;28(12):993-6. doi: 10.1046/j.1440-1681.2001.03584.x.

Abstract
  1. Adrenocorticotrophic hormone (ACTH) raises blood pressure in humans, sheep, rat and mouse. In rat and humans, but not sheep, the hypertension can be explained by glucocorticoid excess. 2. In both rat and humans, the hypertension is associated with a rise in cardiac output and renal vascular resistance. 3. In both rat and humans, the nitric oxide system is implicated in glucocorticoid hypertension. 4. In both rat and humans, hypertension due to naturally occurring glucocorticoids is not prevented by drugs that block classical glucocorticoid or mineralocorticoid receptors. 5. Abnormalities in glucocorticoid metabolism may contribute to some forms of 'essential' hypertension.
摘要
  1. 促肾上腺皮质激素(ACTH)可使人类、绵羊、大鼠和小鼠的血压升高。在大鼠和人类中,而非绵羊中,高血压可由糖皮质激素过量来解释。2. 在大鼠和人类中,高血压均与心输出量增加和肾血管阻力升高有关。3. 在大鼠和人类中,一氧化氮系统都与糖皮质激素性高血压有关。4. 在大鼠和人类中,由天然存在的糖皮质激素引起的高血压不能被阻断经典糖皮质激素或盐皮质激素受体的药物所预防。5. 糖皮质激素代谢异常可能导致某些形式的“原发性”高血压。

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