Melatonin, mitochondria and hypertension

Melatonin, due to its multiple means and mechanisms of action, plays a fundamental role in the regulation of the organismal physiology by fine tunning several functions. The cardiovascular system is an important site of action as melatonin regulates blood pressure both by central and peripheral inte...

Full description

Saved in:
Bibliographic Details
Published inCellular and molecular life sciences : CMLS Vol. 74; no. 21; pp. 3955 - 3964
Main Authors Baltatu, Ovidiu C., Amaral, Fernanda G., Campos, Luciana A., Cipolla-Neto, Jose
Format Journal Article
LanguageEnglish
Published Cham Springer International Publishing 01.11.2017
Springer Nature B.V
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:Melatonin, due to its multiple means and mechanisms of action, plays a fundamental role in the regulation of the organismal physiology by fine tunning several functions. The cardiovascular system is an important site of action as melatonin regulates blood pressure both by central and peripheral interventions, in addition to its relation with the renin–angiotensin system. Besides, the systemic management of several processes, melatonin acts on mitochondria regulation to maintain a healthy cardiovascular system. Hypertension affects target organs in different ways and cellular energy metabolism is frequently involved due to mitochondrial alterations that include a rise in reactive oxygen species production and an ATP synthesis decrease. The discussion that follows shows the role played by melatonin in the regulation of mitochondrial physiology in several levels of the cardiovascular system, including brain, heart, kidney, blood vessels and, particularly, regulating the renin–angiotensin system. This discussion shows the putative importance of using melatonin as a therapeutic tool involving its antioxidant potential and its action on mitochondrial physiology in the cardiovascular system.
Bibliography:ObjectType-Article-2
SourceType-Scholarly Journals-1
ObjectType-Feature-3
content type line 23
ObjectType-Review-1
ISSN:1420-682X
1420-9071
DOI:10.1007/s00018-017-2613-y