Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Comparative Study
. 2006 Jun 15;88(1-2):95-100.
doi: 10.1016/j.physbeh.2006.03.008. Epub 2006 Apr 27.

Salt consumption increases blood pressure and abolishes the light/dark rhythm in angiotensin AT1a receptor deficient mice

Affiliations
Comparative Study

Salt consumption increases blood pressure and abolishes the light/dark rhythm in angiotensin AT1a receptor deficient mice

Yanfang Chen et al. Physiol Behav. .

Abstract

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.

PubMed Disclaimer

Similar articles

Cited by

Publication types

Substances

LinkOut - more resources