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Brainstem hypoperfusion as a causative mechanism for neurogenic hypertension

66 months
Approved budget:
Dr Fiona McBryde
Health issue:
Metabolic and endocrine (excl. diabetes and bone)
Proposal type:
Sir Charles Hercus Fellowship
Lay summary
This award will enable me to establish international research collaborations from New Zealand. Mechanisms regulating the long term control of arterial pressure remain incompletely understood. With significant numbers of hypertensive patients, this has important clinical and financial implications. I hypothesise that hypertension is triggered by brainstem hypoperfusion, thereby ensuring adequate brain perfusion. In hypertensive humans vertebrobasilar artery resistance is increased. Firstly, I will establish that elevated cerebrovascular resistance (CVR) induces hypertension in the rat. The potential mechanisms underlying both the hypertensive response to chronic hypoperfusion, and the events permitting any arterial pressure recovery will be assessed in normotensive and hypertensive rats. The autonomic innervation of cerebral circulation will be electrically and genetically modulated to understand its role in structural re-modelling and increase therapeutic consequences for arterial pressure. These findings will establish whether elevated CVR in the brainstem causes hypertension, which may then permit translational trials to better control human hypertension.