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AssigneesThomas Jefferson University, Nova Southeastern University
InventorsAnastasios Lymperopoulos, Walter J. Koch
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The disclosure describes the contribution of elevated levels of circulating alsosterone to heart disease and other hyperaldosteronic conditions. Since activation of beta-arrestin I (beta.arr-1) by the Angiotensin II (AngII) type 1 receptor (AT1R) mediates AngII-induced aldosterone production, beta-arrestin I (beta.arr-1) is a therapeutic target for heart disease. Specifically, the disclosure provides a beta.arr-1 protein fragment comprising the C-terminus of beta.arr-1 (beta.arr1ct; SEQ ID NO:3), compositions containing this protein fragment, and methods of using this protein fragment to reduce elevated levels of aldosterone in heart disease and other hyperaldosteronic conditions by inhibition of beta-arrestin (beta.arr-1). These compositions and methods are of therapeutic benefit in chronic heart failure and progression to heart failure after myocardial infarction (MI). Additionally, the invention provides an AngII peptide analog (SEQ ID NO:4), compositions containing this analog, and methods of using this analog for stimulation of beta.arr-1 activity and aldosterone production.
A method for reducing plasma aldosterone level in a patient comprising inhibiting adrenal β-arrestin-1 (βaar1).
A method for inhibiting adrenal β-arrestin-1 (βaar1) in a patient having a hyperaldosteronic condition comprising overexpressing a βarr1 protein fragment comprising a C-terminus of βarr1 (βarr1ct).
A composition for treatment of a hyperaldosteronic condition comprising a βarr1 protein fragment including a C-terminus of βarr1 (βarr1ct).
A method for increasing angiotensin II-dependent β-arrestin activity in a patient comprising administering a therapeutically-effective amount of an angiotensin II (AngII) biased agonist to the patient, wherein the AngII agonist is an AngII peptide analog.
Dependencies are inferred from the claim text.