Regulation of Biogenesis and Fusion/Fission Processes of Vascular Mitochondria In Aldosterone-Induced Hypertension
Elena Olivares-Álvaro, María Belén Ruiz-Roso, Mercedes Klett-Mingo, Sandra Ballesteros, Ricardo Gredilla, Adrián Galiana-Simal, Natalia de las Heras, Vicente Lahera, Beatriz Martín-Fernández*
Identifiers and Pagination:Year: 2018
First Page: 76
Last Page: 85
Publisher Id: TOHYPERJ-10-76
Article History:Received Date: 29/8/2018
Revision Received Date: 15/10/2018
Acceptance Date: 31/10/2018
Electronic publication date: 28/12 /2018
Collection year: 2018
open-access license: This is an open access article distributed under the terms of the Creative Commons Attribution 4.0 International Public License (CC-BY 4.0), a copy of which is available at: (https://creativecommons.org/licenses/by/4.0/legalcode). This license permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Aldosterone plays a key role in the development of endothelial dysfunction and hypertension. The regulation of biogenesis and fusion/fission processes of vascular mitochondria has not been examined in aldosterone-induced hypertension. Thereby, we sought to explore in greater depth the role of aldosterone in mitochondrial biogenesis and fusion/fission processes in hypertension and the associated increases in oxidative stress.
Male Wistar rats received aldosterone (1mg/Kg/day) + 1% NaCl as drinking water for 3 weeks.
Systolic blood pressure was elevated (p<0.05) in aldosterone-treated rats. eNOS and p-eNOSSer1177 protein expression was down regulated (p<0.05) and NADPH oxidase subunit p22phox expression was increased (p<0.05) in aldosterone-treated rats. Expression of mitochondrial biogenesis proteins SIRT1, PGC1α, PPARγ, and TFAM decreased (p<0.05) in aldosterone-treated rats. Protein expression of vascular DRP1, OMA1 and S-OPA1 up regulated (p<0.05) in aldosterone-treated rats. MFN1 and L-OPA1 (p<0.05) decreased in aldosterone-treated animals.
The results showed that, in aldosterone-treated rats, hypertension is likely associated with increased oxidative stress in the aorta and with changes in the regulation of two key mitochondrial processes such as biogenesis and fusion/fission processes. The overall mitochondrial alterations observed in the study may play a role in aldosterone-derived vascular oxidative stress and hypertension.