Salt consumption increases blood pressure and abolishes the light/dark rhythm in angiotensin AT1a receptor deficient mice.
Salt consumption increases blood pressure and abolishes the light/dark rhythm in angiotensin AT1a receptor deficient mice.
复制标题
血管紧张素 AT1a 受体缺陷小鼠的食盐摄入会增加血压并消除光/暗节律。
DOI：
10.1016/j.physbeh.2006.03.008
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发表时间：
2006
期刊：
影响因子：
--
通讯作者：
Morris,Mariana
中科院分区：
文献类型：
--
作者：
Chen,Yanfang;Oroszi,TerryL;Morris,Mariana
Experiments were performed to study the role of angiotensin (Ang) AT1a receptors in dietary sodium-induced changes in blood pressure (BP). We measured light/dark rhythms in BP, heart rate (HR) and drinking behavior in Ang AT1a deficient (AT1a −/−) and wild type (AT1a +/+) mice with arterial telemetric catheters. Mice were given ad libitum access to a high salt diet (8% NaCl, HSD for 8 days) and tap water. The major finding was that the Ang AT1a −/− mice showed enhanced sodium sensitivity. This was seen by a greater percentage increase in BP (+21% vs. +12%) and an earlier onset of BP change (increase on day 5 vs. day 8) in AT1a −/− vs. AT1a +/+. The normal light/dark BP rhythm was abolished in AT1a −/− after 5 days of HSD. HSD produced an increase in water intake (drinking activity and volume consumed) in both groups with no difference in the percentage increase or the light/dark drinking rhythm. HSD produced no changes in plasma osmolality, hematocrit or body weight in either group. Evidence shows that a deficiency of Ang AT1a receptors results in an enhancement in sodium sensitivity along with a disruption of the normal light/dark BP rhythm. The data combined with previous findings suggests that activation of other components of the renin angiotensin system and/or sympathetic pathways may be responsible for the cardiovascular changes in AT1a deficient mice.
