Importance of the medial amygdala to the neurogenic hypertension in Schlager mice

Abstract

Schlager BPH mice are hypertensive due to an overactive sympathetic nervous system (SNS) and that is associated with over activity of the medial amygdala (MeAm). To determine whether the MeAm is responsible for the hypertension, we assessed the effect of MeAm ablation on blood pressure (BP) and stress reactivity. Radio‐telemetry devices were implanted in 10 normotensive (BPN) and 8 BPH mice and the MeAm was lesioned with bilateral ibotenic acid injections. One week before and 3 weeks after lesion surgery, BP was measured for 48hrs and restraint stress performed. During control measurements, BP was 121±4mmHg in BPH versus 101±2mmHg in BPN mice (P<0.001). MeAm lesions reduced 24hr BP, −11±5mmHg (P = 0.003) in BPH mice and had no effect in BPN mice. The lesion effect was similar during both day and night, suggesting a contribution independent of the state of arousal. Despite reductions in BP, the pressor response to restraint stress was well maintained. Spectral analysis revealed a reduction in low frequency mean arterial pressure (MAP) power after MeAm lesions in BPH/2J (P<0.05) suggesting that the lesions reduced SNS activity. These results show that tonic activation of the MeAm contributes at least 50% of the hypertension in BPH mice through pathways that involve activation of the SNS but which are independent of those regulating the state of arousal or the cardiovascular response to stress. Supported by NHMRC Australia