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Am J Physiol Heart Circ Physiol. 2013 Nov 15;305(10):H1417-27. doi: 10.1152/ajpheart.00089.2013. Epub 2013 Sep 16.

Role of mitochondrial oxidative stress in hypertension.

Author information

1
Division of Clinical Pharmacology, Free Radicals in Medicine Core, Vanderbilt University Medical Center, Nashville, Tennessee; and.

Abstract

Based on mosaic theory, hypertension is a multifactorial disorder that develops because of genetic, environmental, anatomical, adaptive neural, endocrine, humoral, and hemodynamic factors. It has been recently proposed that oxidative stress may contribute to all of these factors and production of reactive oxygen species (ROS) play an important role in the development of hypertension. Previous studies focusing on the role of vascular NADPH oxidases provided strong support of this concept. Although mitochondria represent one of the most significant sources of cellular ROS generation, the regulation of mitochondrial ROS generation in the cardiovascular system and its pathophysiological role in hypertension are much less understood. In this review, the role of mitochondrial oxidative stress in the pathophysiology of hypertension and cross talk between angiotensin II signaling, pathways involved in mechanotransduction, NADPH oxidases, and mitochondria-derived ROS are considered. The possible benefits of therapeutic strategies that have the potential to attenuate mitochondrial oxidative stress for the prevention/treatment of hypertension are also discussed.

KEYWORDS:

antioxidant; hypertension; mitochondria; oxidative stress; superoxide

PMID:
24043248
PMCID:
PMC3840266
DOI:
10.1152/ajpheart.00089.2013
[Indexed for MEDLINE]
Free PMC Article

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