Role of Indapamide in Attenuating Pressure Overload-Induced Left Ventricular Hypertrophythrough Modulation of the Cardiac Renin-Angiotensin System
Main Article Content
Abstract
In rat hearts under continuous pressure overload, the hypertension diuretic medication indapamide changed the structure of the left ventricle (LV). Banding the ascending aorta increased LV pressure and, consequently, LV
mass throughout a 6-week period. For an extra 6 weeks, the mice were given either a low-dose (1 mg/kg/day, n = 9) or a high-dose (10 mg/kg/day, n = 9) of indapamide. When compared to vehicle-treated controls, low-
dose indapamide treatment decreased LV weights. In addition, low-dose indapamide therapy improved molecular indicators of hypertrophy, such as LV atrial natriuretic factor mRNA expression, and decreased myocyte volume. Furthermore, LV angiotensin-converting enzyme and plasma were significantly reduced by low-dose indapamide (−65%). Despite the LV’s continuous pressure overload and the fact that long-term low-dose indapamide therapy did not considerably change salt excretion, these changes were seen. LV mass, shape, or gene expression were not significantly affected by high-dose indapamide treatment. In conclusion, in rats with persistent LV pressure- overload, low-dose indapamide administration results in a slight regression of ventricular hypertrophy and a downregulation of cardiac renin-angiotensin system components
Article Details
Section
This work is licensed under a Creative Commons Attribution 4.0 International License.
This is an Open Access article distributed under the terms of the Attribution-Noncommercial 4.0 International License [CC BY-NC 4.0], which requires that reusers give credit to the creator. It allows reusers to distribute, remix, adapt, and build upon the material in any medium or format, for noncommercial purposes only.