RESEARCH ARTICLE


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*
Department of Physiology, Faculty of Medicine, Universidad Complutense. 28040, Madrid, Spain.

Article Information


Identifiers and Pagination:

Year: 2018
Volume: 10
First Page: 76
Last Page: 85
Publisher Id: TOHYPERJ-10-76
DOI: 10.2174/1876526201810010076

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

© 2018 Olivares-Álvaro et al.

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.

* Address correspondence to this author at the Department of Physiology, Faculty of Medicine, Universidad Complutense. 28040, Madrid, Spain, Tel: 34 91 394-1490, Fax: 34 91 3941628; E-mail: bmartinfernandez@med.ucm.es


Abstract

Background:

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.

Methods:

Male Wistar rats received aldosterone (1mg/Kg/day) + 1% NaCl as drinking water for 3 weeks.

Results:

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.

Conclusion:

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.

Keywords: Vascular, Mitochondria, Aldosterone, Oxidative stress, Hypertension, Endothelial nitric oxide synthase (eNOS).