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Schlager inbred hypertensive mice (BPH/2J) have been suggested to have high blood pressure (BP) due to an overactive sympathetic nervous system (SNS). The brain nuclei associated with the hypertension are also those involved in the integration of the cardiovascular responses to stress. Therefore, in the present study, we hypothesize that an increased contribution of the SNS in BPH/2J mice may culminate in a greater pressor response to stressful stimuli in these hypertensive mice than normotensive (BPN/3J) mice.Male hypertensive BPH/2J and normotensive BPN/3J mice were implanted with telemetry devices and exposed to a series of behavioral “stress” tests including aversive stress (shaker, clean cage switch, and restraint) and nonaversive stress (feeding).Aversive stress caused a 67-88% greater pressor response in BPH/2J compared with BPN/3J mice. By contrast, the feeding-induced pressor response was not different between groups. All stressors induced tachycardia that was less in BPH/2J mice (feeding and restraint) and others were not different between groups (clean cage switch and shaker).These findings indicate that hypertension in BPH/2J mice is associated with greater pressor responsiveness to aversive stress but not to appetitive arousal. Thus, BPH/2J hypertensive mice may be a particularly relevant model for human hypertensive patients that overrespond to daily stressors.