Salt consumption increases blood pressure and abolishes the light/dark rhythm in angiotensin AT1a receptor deficient mice.
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.
Chen
Yanfang
Y
Department of Pharmacology and Toxicology, Boonshoft School of Medicine, Wright State University School, Dayton, OH 45450, USA. yanfang.chen@wright.edu
Oroszi
Terry L
TL
Morris
Mariana
M
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects*; D001835:Body Weight / Q000187:drug effects / Q000235:genetics; D002940:Circadian Rhythm / Q000187:drug effects* / Q000502:physiology; D004326:Drinking / Q000187:drug effects; D004327:Drinking Behavior / Q000187:drug effects; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D008297:Male; D051379:Mice; D018345:Mice, Knockout; D044140:Receptor, Angiotensin, Type 1 / Q000172:deficiency*; D017673:Sodium Chloride, Dietary / Q000008:administration & dosage*; D013997:Time Factors
D044140:Receptor, Angiotensin, Type 1; D017673:Sodium Chloride, Dietary