Inhibition of low grade inflammation in the brain to reduce blood pressure

Years funded:
2019

In around 10% of people diagnosed with high blood pressure even the combination of three or more drugs does not lower the blood pressure to normal levels. The mechanisms underlying high blood pressure are multivariate and current evidence derived primarily from experimental studies suggest a potential causative role of the immune system in this scenario. The immune-mediated inflammatory environment exaggerates the activity of the sympathetic nervous system which is a major driver of sustained blood pressure elevation. 

Whether immune mechanisms play an important role  in human hypertension has not yet been adequately investigated. To fill this knowledge gap and to explore whether therapeutic targeting of relevant immune mechanism has the potential to lower BP and the associated organ damage, we will conduct a unique series of human studies applying state-of-the-art methodology to investigate the potential link between blood pressure, immune system mediated inflammatory processes, and sympathetic nervous system activity  By breaking this vicious cycle via inhibition of brain inflammation with the anti-inflammatory drug minocycline, it should be possible to reduce BP and prevent end organ damage in hypertensive patients.

This study follows a ‘randomized, double-blind, placebo controlled, parallel group design’ where we aim to demonstrate that in patients with uncontrolled hypertension despite the use of multiple drugs,  oral treatment with minocycline results in reduced sympathetic nerve activity and concomitant lowering of blood pressure. This conceptual study, if positive, will pave way for future larger randomized controlled trials and may lead to identification of preferred immune targets for blood pressure lowering.

Researcher Profile

Professor Markus Schlaich

Institute: University of Western Australia
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