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Our objective

We aim to understand how PACAP drives the sympathetically mediated increases in blood glucose and blood pressure in models of sleep apnoea. This will be addressed using physiological, pharmacological and optogenetic methods in vivo models, as well as molecular and histochemical/anatomical and proteomic approaches.

Our impact

Cardiovascular disease (CVD) is the principal cause of death in the world. Intriguingly, 10% of CVD is now attributed to obstructive sleep apnoea (OSA), a condition characterised by intermittent episodes of hypoxia during sleep, and evident in >10% of the population. The most plausible link between OSA and CVD is that in OSA, intermittent activation of chemoreceptors leads to sympathoexcitation that results in hypertension and diabetes.

Our research will uncover fundamental mechanisms driving the cardiometabolic effects of OSA, and these results have the potential to spearhead development of new strategies for treating OSA, such as receptor-selective antagonists or targeted gene therapy to dramatically improve metabolic function in OSA sufferers.

The team


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