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α-肾上腺素能(去甲肾上腺素)对抗利尿激素活性的影响。

alpha-Adrenergic (norepinephrine) effect on antidiuretic hormone activity.

作者信息

Klein L A

出版信息

Invest Urol. 1975 Sep;13(2):159-64.

PMID:1184340
Abstract

The mechanism by which norepinephrine (NE) inhibits the antidiuretic activity of anti-diuretic hormone (ADH) was studied in anesthetized normal and ADH-deficient rats. NE infusion increased aortic blood pressure and resulted in increased urine volume and sodium and potassium excretion without changes in creatinine excretion. p-Aminohippuric acid excretion did not change in normals and rose (from 34 +/- 9 to 51 +/- 11, P less than 0.025) in ADH-deficient rats. Urine osmolality fell in normals (from 363 +/- 29 to 298 +/- 42, P less than 0.05) but not in ADH deficients (from 332 +/- 29 to 363 +/- 26, p less than 0.1). ADH-deficient rats given 50 muU per kg-min of ADH intravenously responded with antidiuresis, including hyperosmolality (from a range of 225 to 240 to a range of 332 to 333, P less than 0.025). When NE was infused at 0.5 mug per kg-min, no inhibition of hyperosmolality was noted but natriuresis and augmented volume excretion occurred. At 1.5 mug per kg-min, NE completely reversed the hyperosmolality induced with ADH. The results suggest that NE-induced pressure diuresis reduces osmolality only when ADH is present in the system and so by competitive inhibition of ADH action on the renal tubule.

摘要

在麻醉的正常大鼠和抗利尿激素(ADH)缺乏的大鼠中,研究了去甲肾上腺素(NE)抑制抗利尿激素(ADH)抗利尿活性的机制。输注NE可升高主动脉血压,并导致尿量增加以及钠和钾排泄增加,而肌酐排泄无变化。对氨基马尿酸排泄在正常大鼠中未改变,而在ADH缺乏的大鼠中升高(从34±9升至51±11,P<0.025)。正常大鼠的尿渗透压下降(从363±29降至298±42,P<0.05),但ADH缺乏的大鼠未下降(从332±29升至363±26,P<0.1)。给ADH缺乏的大鼠静脉注射每千克体重每分钟50微单位的ADH后出现抗利尿反应,包括高渗(从225至240的范围升至332至333的范围,P<0.025)。当以每千克体重每分钟0.5微克的速度输注NE时,未观察到对高渗的抑制作用,但出现了利钠作用和尿量排泄增加。当以每千克体重每分钟1.5微克的速度输注NE时,NE完全逆转了由ADH诱导的高渗。结果表明,NE诱导的压力性利尿仅在系统中存在ADH时才降低渗透压,因此是通过竞争性抑制ADH对肾小管的作用来实现的。

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