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动脉血压对血管紧张素II引起的饮水和排尿反应的影响。

Effect of arterial pressure on drinking and urinary responses to angiotensin II.

作者信息

Evered M D, Robinson M M, Rose P A

机构信息

Department of Physiology, University of Saskatchewan, Saskatoon, Canada.

出版信息

Am J Physiol. 1988 Jan;254(1 Pt 2):R69-74. doi: 10.1152/ajpregu.1988.254.1.R69.

DOI:10.1152/ajpregu.1988.254.1.R69
PMID:3337271
Abstract

To investigate the relationship between angiotensin II (ANG II) and mean arterial pressure (MAP) in the control of drinking in rats, we infused ANG II intravenously at constant rates (either 50 or 100 ng.kg-1.min-1 for 90 min) and varied MAP by intravenous injections of diazoxide (5-20 mg/kg). Rats were pretreated with captopril to block the endogenous synthesis of ANG II. When given alone, low and high doses of ANG II increased MAP approximately 30 and 50 mmHg, respectively. The low but not the high dose significantly increased water intake above control levels. Both doses caused such a large diuresis and natriuresis that the net effect was fluid loss. Reducing MAP toward normal greatly increased the drinking response to the high but not the low dose of ANG II and reduced the urinary solute and water loss to both doses. These results support the hypothesis that water intake and net fluid gain are inhibited when MAP is above normal. When MAP was reduced below normal in rats given constant infusions of ANG II the amount of water drunk and net fluid gain was proportional to the dose of ANG II but not the dose of diazoxide, the degree of hypotension, or urinary losses. This is consistent with previous reports that ANG II is essential for the drinking response to hypotension. Furthermore, it demonstrates that ANG II is not merely permissive but probably the signal controlling water intake when arterial pressure is reduced below normal.

摘要

为了研究血管紧张素II(ANG II)与平均动脉压(MAP)在大鼠饮水控制中的关系,我们以恒定速率静脉注射ANG II(50或100 ng·kg-1·min-1,持续90分钟),并通过静脉注射二氮嗪(5 - 20 mg/kg)来改变MAP。大鼠预先用卡托普利处理以阻断ANG II的内源性合成。单独给予时,低剂量和高剂量的ANG II分别使MAP升高约30和50 mmHg。低剂量而非高剂量显著增加了饮水量,使其高于对照水平。两种剂量均引起大量利尿和利钠,以至于净效应是体液丢失。将MAP降至正常水平极大地增加了对高剂量而非低剂量ANG II的饮水反应,并减少了两种剂量下的尿溶质和水分丢失。这些结果支持以下假设:当MAP高于正常时,水摄入和净体液增加受到抑制。当在持续输注ANG II的大鼠中使MAP降至正常水平以下时,饮水量和净体液增加量与ANG II的剂量成正比,而与二氮嗪的剂量、低血压程度或尿丢失量无关。这与先前的报道一致,即ANG II对于低血压引起的饮水反应至关重要。此外,这表明当动脉压降至正常水平以下时,ANG II不仅是允许性的,而且可能是控制水摄入的信号。

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