Myocardial Implications in Renin Angiotensin Aldosterone-Regulated Hypertension
Author
Byrum, Rachel
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This item will be available on: 2025-07-01
Abstract
Hypertension 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.
Date
2023-08-08
Citation:
APA:
Byrum, Rachel.
(August 2023).
Myocardial Implications in Renin Angiotensin Aldosterone-Regulated Hypertension
(Master's Thesis, East Carolina University). Retrieved from the Scholarship.
(http://hdl.handle.net/10342/13165.)
MLA:
Byrum, Rachel.
Myocardial Implications in Renin Angiotensin Aldosterone-Regulated Hypertension.
Master's Thesis. East Carolina University,
August 2023. The Scholarship.
http://hdl.handle.net/10342/13165.
June 29, 2024.
Chicago:
Byrum, Rachel,
“Myocardial Implications in Renin Angiotensin Aldosterone-Regulated Hypertension”
(Master's Thesis., East Carolina University,
August 2023).
AMA:
Byrum, Rachel.
Myocardial Implications in Renin Angiotensin Aldosterone-Regulated Hypertension
[Master's Thesis]. Greenville, NC: East Carolina University;
August 2023.
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Publisher
East Carolina University