• DOI:10.1152/AJPREGU.00306.2004
• Corpus ID: 10813832

Sympathetic and angiotensin-dependent hypertension during cage-switch stress in mice.

@article{Lee2004SympatheticAA,
  title={Sympathetic and angiotensin-dependent hypertension during cage-switch stress in mice.},
  author={Dexter L. Lee and R. Clinton Webb and Michael W. Brands},
  journal={American journal of physiology. Regulatory, integrative and comparative physiology},
  year={2004},
  volume={287 6},
  pages={
          R1394-8
        }
}

• Dexter L. Lee, R. Webb, M. Brands
• Published 1 December 2004
• Biology, Medicine
• American journal of physiology. Regulatory, integrative and comparative physiology

The goal of this study was to determine the dependence of the acute hypertensive response to a novel model of acute psychosocial stress on the sympathetic and renin-angiotensin systems. Baseline mean arterial pressure (MAP), heart rate (HR), and locomotor activity were measured with telemetry in mice for a 1-h period and averaged 98 +/- 1 mmHg, 505 +/- 3 beats/min, and 5 +/- 1 counts, respectively. Stress was induced by placing a mouse into a cage previously occupied by a different male mouse, and this increased MAP, HR, and activity in the control group by 40 +/- 2 mmHg, 204 +/- 25 beats/min, and 68 +/- 6 counts, respectively. Each variable gradually returned to baseline levels by 90 min after beginning cage switch. Pretreatment with terazosin (10 mg/kg ip) significantly reduced the initial increase in MAP to 12 +/- 6 mmHg, whereas MAP for the last 45 min was superimposable on control values. Atenolol (10 mg/ml drinking water) had no effect to blunt the initial increase in MAP but had a growing effect from 10 min onward, decreasing MAP all the way to baseline by 60 min after starting cage switch. Captopril (2 mg/ml drinking water) treatment caused a very similar response. All three treatments significantly decreased the area under the blood pressure curve, and the blood pressure effect could not be attributed uniformly to effects on HR or activity. These data suggest that our novel model of psychosocial stress causes an initial alpha(1)-receptor-dependent increase in MAP. The later phase of the pressor response is blocked similarly by a beta(1)-receptor antagonist and an ACE inhibitor, independent of HR, suggesting that the beta(1)-dependent blood pressure effect is due, in large part, to the renin-angiotensin system.