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Project leader: Kristy Jackson

We discovered that the Schlager hypertensive BPH/2J mouse has a neurogenic form of hypertension characterised by an exaggerated blood pressure response to stress and also a much greater cardiovascular circadian rhythm. Both of these are accompanied by a much greater activity of neurons in the amygdala and hypothalamus. The hypertension can be blocked by inhibiting the sympathetic nervous system (SNS) and also by specific lesions of the medial amygdala. We recently identified that a specific region of the amygdala is the cause of a tonic activation of the SNS explaining most of the hypertension and that the mechanism involves inhibitory GABAA receptors. We also discovered that BPH mice have a greater dependence on the renin angiotensin system (RAS) that is associated with higher levels of renin mRNA due to less microRNA (miR-181a) in the kidney. We are currently investigating these central mechanisms, pathways and neuromodulators as well as the connection between the SNS and renal mechanisms contributing to hypertension in BPH mice.

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