Myocardial Implications in Renin Angiotensin Aldosterone-Regulated Hypertension

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dc.contributor.advisorAbles, Elizabeth Tweedie
dc.contributor.authorByrum, Rachel
dc.contributor.departmentBiology
dc.date.accessioned2023-09-14T13:14:21Z
dc.date.created2023-07
dc.date.issued2023-08-08
dc.date.submittedJuly 2023
dc.date.updated2023-09-12T17:51:14Z
dc.degree.departmentBiology
dc.degree.disciplineMS-Molecular Biology & Biotech
dc.degree.grantorEast Carolina University
dc.degree.levelMasters
dc.degree.nameM.S.
dc.description.abstractHypertension is a prevalent and potentially deadly disease that affects approximately 116 million (47%) adults diagnosed in the U.S. as reported by the CDC in 2017. Understanding mechanisms responsible for high blood pressure, particularly, the Renin-Angiotensin-Aldosterone System (RAAS) may lead to better treatment options and preventative measures. The current study determines the local role of RAAS on heart muscle and evaluates the indirect Ca2+ homeostatic control of cardiac contractility during high blood pressure. The objectives are to study the expression of RAAS-mediated receptors and the membrane-bound Na/K ATPase (NKA) pump as it relates to the membrane-bound Sodium-Calcium exchanger (NCX). We assess the intracellular sarco/endoplasmic reticulum Ca2+-ATPase (SERCA) in the ventricular myocytes for calcium reuptake since NKA in association with NCX and SERCA may play a significant role in ventricular contractility. The results show a significant decrease in the protein expression for G protein-coupled receptor (GPCR), MAS1 proto-oncogene protein (MAS) for angiotensin 1-7 (Ang1-7) peptides in hypertension. Conversely, protein expression for angiotensin receptor type 1 (AT1R) was significantly higher in cardiomyocytes. While AT1R mediates the enhancement of cardiac contractility, MAS receptor mediates the metabolite of angiotensin II, through Ang1-7, and serves as the protective arm of angiotensin peptides. Further, the results show an increase in protein expression of cardiac membrane-bound NKA isoforms (1 and 2) in the hypertensive rodents, believed to have triggered intracellular calcium ([Ca2+] i) increase via NCX system. In addition, there was a diminution in Ca2+ reuptake pump by SERCA in the sarcoplasmic reticulum (SR) of cardiomyocytes in hypertensive rodents. This could explain increased contractility of the cardiomyocytes through excitation-contraction coupling and calcium-induced calcium release (CICR) mechanisms. The study is a groundwork understanding of cardiac dysfunction during hypertension and may lead to a treatment option and/or preventative measures for sustained blood pressure.
dc.embargo.lift2025-07-01
dc.embargo.terms2025-07-01
dc.format.mimetypeapplication/pdf
dc.identifier.urihttp://hdl.handle.net/10342/13165
dc.language.isoen
dc.publisherEast Carolina University
dc.subjectRenin Angiotensin Aldosterone System
dc.subjectCalcium Homeostasis
dc.subjectAngiotensin II, Angiotensin (1-7)
dc.subjectCardiomyocytes
dc.subjectHypertension
dc.subjectHigh blood pressure
dc.subject(mREN2)27
dc.titleMyocardial Implications in Renin Angiotensin Aldosterone-Regulated Hypertension
dc.typeMaster's Thesis
dc.type.materialtext

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