Hypertension is central in determining cardiovascular risk and is a potent indicator of morbidity and mortality; however, there is an unmet clinical need for disease-modifying and prophylactic interventions. Our research group addresses this by investigating the processes that modulate sympathetic activity and my research aims to identify novel targets within the cardiac-sympathetic ganglia, that may translate from bench to bedside1-3.
Dysautonomia is a well-established contributor to the development and progression of clinical hypertension and many other cardiovascular diseases. Sympathetic hyperactivity and vagal impairment are features of human hypertension as well as in subjects with a familial predisposition for hypertension. This neural phenotype is highly conserved and also observed in the spontaneously hypertensive rat (SHR) as well as young normotensive SHR (proSHR).
My research aims to understand the key processes involved in sympathetic hyperactivity and the molecular mechanisms that impair sympathetic-cardiac communication. The primary goal is to establish how these processes are altered in cardiac disease, to identify novel targets for the future development of effective clinical anti-hypertensive treatments.
1. Bardsley EN, Larsen HE, Paterson DJ. Impaired cAMP-cGMP cross-talk during cardiac sympathetic dysautonomia. Channels (Austin). November 2016:1-3. doi:10.1080/19336950.2016.1259040.
2. Larsen HE, Bardsley EN, Lefkimmiatis K, Paterson DJ. Dysregulation of Neuronal Ca2+ Channel Linked to Heightened Sympathetic Phenotype in Prohypertensive States. Journal of Neuroscience. 2016;36(33):8562-8573. doi:10.1523/JNEUROSCI.1059-16.2016.
3. Bardsley E, Paterson DJ. Impaired Cyclic Nucleotide Signalling in Pre-Hypertensive Spontaneously Hypertensive Rats: A Dichotomy of Pathways? The FASEB Journal. 2016;30(1 Supplement):1006.5-1006.5.