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AAS-Lundbeck Research Fellowship

Congratulations to our recent AAS-Lundbeck Research Fellowship awardees.


Dr. Jhansi Dyavanapalli

 

Title: Can oxytocin restore parasympathetic activity to the heart in heart failure
Awardee: Dr. Jhansi Dyavanapalli
Mentor: Dr. David Mendelowitz

 
Summary
 
Heart failure is a widespread and debilitating cardiovascular disease that affects nearly 23 million people worldwide with approximately 2 million new patients diagnosed annually. A distinctive hallmark of heart failure is autonomic imbalance, consisting of increased sympathetic activity and decreased parasympathetic tone.
 
The studies in this proposal will either support or refute the hypothesis that oxytocin neuron activation can restore diminished parasympathetic cardiac activity and blunt the deleterious cardiac function alterations that occur in animals with left ventricular hypertrophy and cardiac dysfunction.
 


Dr. Robert Larson

 

Title: Targeting Cardiac Sympathetic and Renin Angiotensin Systems with Ang-(1-7) in Hypertrophic Cardiomyopathy
Awardee: Dr. Robert Larson
Mentor: Dr. Mark Chapleau

 
Summary
 
Hypertrophic cardiomyopathy (HCM) is a relatively common inherited disease characterized by cardiac hypertrophy (enlarged heart), fibrosis, and dysfunction. Patients with HCM exhibit abnormal neural reflex control of blood pressure and heart rate, and are at high risk of developing heart failure, arrhythmias and sudden cardiac death. Current treatment strategies primarily target symptoms and not development of the disease. We propose a novel treatment strategy with Angiotensin-(1-7), a peptide known to diminish sympathetic nerve activity and the pro-fibrotic and pro-hypertrophic actions of angiotensin II. We hypothesize that a combination of sustained inhibition of cardiac sympathetic activity and inhibition of adverse cardiac actions of angiotensin II will act synergistically to prevent or reverse cardiac fibrosis, hypertrophy and arrhythmias in HCM. We will test this hypothesis using an established mouse model of HCM, in which a human mutation is targeted selectively to the heart.
 


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