TY - JOUR
T1 - Sympathetic and angiotensin-dependent hypertension during cage-switch stress in mice
AU - Lee, Dexter L.
AU - Webb, R. Clinton
AU - Brands, Michael W.
PY - 2004/12
Y1 - 2004/12
N2 - 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 α1-receptordependent increase in MAP. The later phase of the presser response is blocked similarly by a β1- receptor antagonist and an ACE inhibitor, independent of HR, suggesting that the β1-dependent blood pressure effect is due, in large part, to the renin-angiotensin system.
AB - 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 α1-receptordependent increase in MAP. The later phase of the presser response is blocked similarly by a β1- receptor antagonist and an ACE inhibitor, independent of HR, suggesting that the β1-dependent blood pressure effect is due, in large part, to the renin-angiotensin system.
KW - Mean arterial pressure
KW - Renin-angiotensin system
KW - Sympathetic nervous system
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U2 - 10.1152/ajpregu.00306.2004
DO - 10.1152/ajpregu.00306.2004
M3 - Article
C2 - 15308486
AN - SCOPUS:8844262936
SN - 0363-6119
VL - 287
SP - R1394-R1398
JO - American Journal of Physiology - Regulatory Integrative and Comparative Physiology
JF - American Journal of Physiology - Regulatory Integrative and Comparative Physiology
IS - 6 56-6
ER -