Reactive oxygen species (ROS) are oxygen derivates and play an active role in vascular biology. These compounds are generated within the vascular wall, at the level of endothelial and vascular smooth muscle cells, as well as by adventitial fibroblasts. Physiologically, ROS generation is counteracted effectively by the rate of elimination. In hypertension, a ROS excess occurs, which is not counterbalanced by the endogenous antioxidant mechanisms, leading to a state of oxidative stress. Angiotensin II, the active peptide of the renin-angiotensin-system (RAS), is a significant stimulus for ROS generation within the vasculature. It was also documented that at the level of subfornical cerebral regions an inappropriate RAS stimulation may lead to an increased vascular sympathetic activity. More recently, in conditions of fetal undernutrition, it was also proposed an increased vascular sympathetic activity secondary to inappropriate RAS activation, leading to the development of hypertension in adult life. The present review will discuss the complex interaction between RAS activation, vascular ROS generation and increased sympathetic outflow in hypertension.

Angiotensin II and vascular damage in hypertension: Role of oxidative stress and sympathetic activation

Masi, Stefano
Primo
Conceptualization
;
Virdis, Agostino
Ultimo
Writing – Original Draft Preparation
2019-01-01

Abstract

Reactive oxygen species (ROS) are oxygen derivates and play an active role in vascular biology. These compounds are generated within the vascular wall, at the level of endothelial and vascular smooth muscle cells, as well as by adventitial fibroblasts. Physiologically, ROS generation is counteracted effectively by the rate of elimination. In hypertension, a ROS excess occurs, which is not counterbalanced by the endogenous antioxidant mechanisms, leading to a state of oxidative stress. Angiotensin II, the active peptide of the renin-angiotensin-system (RAS), is a significant stimulus for ROS generation within the vasculature. It was also documented that at the level of subfornical cerebral regions an inappropriate RAS stimulation may lead to an increased vascular sympathetic activity. More recently, in conditions of fetal undernutrition, it was also proposed an increased vascular sympathetic activity secondary to inappropriate RAS activation, leading to the development of hypertension in adult life. The present review will discuss the complex interaction between RAS activation, vascular ROS generation and increased sympathetic outflow in hypertension.
2019
Masi, Stefano; Uliana, Monica; Virdis, Agostino
File in questo prodotto:
Non ci sono file associati a questo prodotto.

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11568/960939
 Attenzione

Attenzione! I dati visualizzati non sono stati sottoposti a validazione da parte dell'ateneo

Citazioni
  • ???jsp.display-item.citation.pmc??? 29
  • Scopus 70
  • ???jsp.display-item.citation.isi??? 66
social impact