Oxidative Stress: A Unifying Paradigm in Hypertension

Area of Science:

• Cardiovascular Science
• Immunology
• Nephrology

Background:

• Hypertension etiology involves genetic, environmental, and pathophysiologic factors.
• Key features include vascular dysfunction, cardiovascular remodelling, renal dysfunction, and sympathetic nervous system activation.
• The immune system plays a significant role, with activated immune cells promoting inflammation and fibrosis.

Purpose of the Study:

• To present a unifying concept of oxidative stress as a central mediator in hypertension.
• To explore novel mechanisms by which reactive oxygen species (ROS) influence hypertension.
• To highlight the roles of ROS in vascular function, aldosterone actions, and immunoinflammation.

Main Methods:

• Review of emerging evidence on oxidative stress and hypertension.
• Focus on the role of NADPH oxidases (Nox) as major ROS sources.
• Analysis of ROS influence on vascular, renal, immune, and cardiovascular systems.

Main Results:

• Oxidative stress, an imbalance favoring oxidants, disrupts redox signaling and causes molecular damage.
• NADPH oxidases (Nox) are identified as the primary sources of ROS in cardiovascular and immune cells.
• Increased Nox expression and activity in hypertension are major contributors to oxidative stress and cardiovascular disease.

Conclusions:

• Oxidative stress is a unifying pathophysiologic process in hypertension.
• ROS generated by Nox significantly contribute to vascular dysfunction, aldosterone/mineralocorticoid effects, and immunoinflammation.
• Targeting Nox-derived oxidative stress may offer novel therapeutic strategies for hypertension.