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The role of immune system in the causation of high blood pressure

Dr Revathy Carnagarin, Institution: University of Western Australia

2019 Postdoctoral Fellowship

Years funded: 2020-2021


Recent evidence suggests an important link between peripheral and central neuro-inflammation, sympathetic activation and blood pressure (BP) elevation. This inflammatory process is immune mediated and affects the regulatory brain nuclei and its interactions with other mediators of cardiovascular regulation, specifically the sympathetic nervous system. The inflammation that occurs in the brain, kidneys and blood vessel wall during hypertension is an important contributor to the sustained elevation in blood pressure and the associated complications and is driven by a vicious cycle of sympathetic nerve activation and immune cell activation.

Importantly, these experimental findings have provided clues about potential mechanisms that could be targeted to test the relevance of the proposed link in humans. These include therapeutic testing of inhibition of neuro-inflammation with minocycline in patients with resistant hypertension, inhibition of T-cell co-stimulation with abatacept, and inhibition of TNF-α activity with etanercept, the latter two in patients with rheumatoid arthritis and hypertension. Reciprocally, targeting central and renal sympathetic drive with renal denervation will allow us to investigate the effect of sympatho-inhibition on both central and organs specific (renal) inflammation. Ultimately, these studies will provide much needed evidence to support an important role of immune mechanisms in human hypertension and the utility of potential therapeutic targets.

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