| First Author | Chen Y | Year | 2006 |
| Journal | Physiol Behav | Volume | 88 |
| Issue | 1-2 | Pages | 95-100 |
| PubMed ID | 16643970 | Mgi Jnum | J:112773 |
| Mgi Id | MGI:3663544 | Doi | 10.1016/j.physbeh.2006.03.008 |
| Citation | Chen Y, et al. (2006) Salt consumption increases blood pressure and abolishes the light/dark rhythm in angiotensin AT1a receptor deficient mice. Physiol Behav 88(1-2):95-100 |
| abstractText | 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. |
