Reactive oxygen species (ROS) are generated by cell metabolism of oxygen and represent signaling molecules playing an active role in vascular biology. In pathological conditions, including hypertension, a ROS excess, together with reduced endogenous antioxidant defenses, occurs, determining a state of oxidative stress. NAD(P)H oxidase (Nox) is a major ROS source within the vasculature. A large body of literature has demonstrated that hypertension-associated vascular functional and structural changes are attributable to Nox-driven intravascular ROS generation. Apocynin is a methoxy-catechol discovered as an inhibitor of superoxide. It has been utilized in several laboratories and in different models of hypertension as an inhibitor of Nox. Recent evidence proposes that apocynin predominantly acts as an antioxidant. The present review will discuss the role of ROS in vascular disease in hypertension and the impact of apocynin on these vascular changes.

Impact of apocynin on vascular disease in hypertension

VIRDIS, AGOSTINO;GESI, MARCO;TADDEI, STEFANO
2016

Abstract

Reactive oxygen species (ROS) are generated by cell metabolism of oxygen and represent signaling molecules playing an active role in vascular biology. In pathological conditions, including hypertension, a ROS excess, together with reduced endogenous antioxidant defenses, occurs, determining a state of oxidative stress. NAD(P)H oxidase (Nox) is a major ROS source within the vasculature. A large body of literature has demonstrated that hypertension-associated vascular functional and structural changes are attributable to Nox-driven intravascular ROS generation. Apocynin is a methoxy-catechol discovered as an inhibitor of superoxide. It has been utilized in several laboratories and in different models of hypertension as an inhibitor of Nox. Recent evidence proposes that apocynin predominantly acts as an antioxidant. The present review will discuss the role of ROS in vascular disease in hypertension and the impact of apocynin on these vascular changes.
Virdis, Agostino; Gesi, Marco; Taddei, Stefano
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/11568/803039
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