ABSENCE OF V1AR ALTERS CARDIAC FUNCTION AT BASELINE AND FOLLOWING ACUTE CARDIAC INJURY

Abstract

Heart failure (HF) is a prevalent disease affecting over 5.1 million people in the United States and over 23 million people worldwide. Many of the symptoms associated with HF are associated with neurohormonal responses to the decrease in cardiac output and systemic blood pressure, such as the activation of the renin-angiotensin-aldosterone system (RAAS) and the sympathetic nervous system. Current treatment guidelines recommend using drugs that block β-adrenergic receptor (βAR) signaling (e.g. β- blockers) or RAAS signaling (e.g. angiotensin receptor blockers/ARBs or angiotensin converting enzyme inhibitors/ACEi’s) Additionally, clinical studies have demonstrated that drugs blocking these neurohormones from properly signaling have decreased hospitalizations, morbidity, and mortality in these HF patients; and these are the only classes of pharmacological therapies that have been shown to reduce patient mortality. Interestingly, the neurohormone arginine vasopressin (AVP) has been implica