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Hypertension is one of the major risk factors for cardiovascular diseases and is considered a leading cause of mortality and morbidity. These diseases affect more than 600 million people worldwide. Within the broader group of hypertensive patients there are subgroups of patients where an associated pathology might drive the hypertension. One such group includes diabetes-associated hypertension and is the focus of this project.

Experimental evidence shows that reactive oxygen species (ROS) play an important role in the pathophysiology of diabetes-associated hypertension. Damage to the vascular endothelium, also known as Endothelial dysfunction (ED), is an early event and a major player in the pathophysiology of hypertension. Recent studies indicate that increased oxidative stress is an important mediator of endothelial injury and patients with hypertension display ED mediated by impaired NO availability as a consequence of oxidative stress. Furthermore, oxidative stress is found to be associated with inflammation and ED in relation to vascular remodeling diabetes-associated hypertension.

We have access to novel activators of the key regulator of oxidative stress, the transcription factor Nrf2 with which to investigate the role of Nrf2 activation in limiting oxidant and inflammatory activities in mouse models of diabetes- associated hypertension. We will investigate this in diabetic Schlager inbred hypertensive mice. Our novel approach has the potential to establish Nrf2 activation as a novel treatment for diabetes-associated hypertension.

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