The Renin-Angiotensin-Aldosterone System as a Therapeutic Target for Endothelial Dysfunction

Abstract

Endothelial dysfunction has been characterized by decreased nitric oxide (NO) synthesis or reduced NO bioavailability, which relates to inflammation, proliferation of smooth muscle cells, deposition of extracellular matrix, vasoconstriction, and a prothrombotic state within the vessel lumen. The endothelium is the site of the final step of synthesis of both NO and angiotensin II (Ang II) and is a major site for their countervailing interaction. Evidence suggests that renin-angiotensin system (RAS) blockade may have an impact on early mechanisms of vascular disease, such as endothelial dysfunction and vascular remodeling that underlie clinical manifestations of cardiovascular disease. This article reviews the current views on the biologic organization of RAS. Evidence supports a pathologic role of RAS activity in promoting endothelial dysfunction characterized by the impairment of NO bioavailability, and provides the basis for considering inhibition of RAS activity as a major target for therapeutic intervention.

Identification of Angiotensin-Converting Enzyme Inhibitory Proteins from Mycelium of Pleurotus pulmonarius (Oyster Mushroom)

“…Nitrite reductase-like protein may contribute to ACE inhibitory activity through the interaction between the NO pathway and RAAS via vascular (endothelial) dysfunction mechanisms [41]. However, there is as yet no supporting data for our hypothesis asserting the synergistic effect of nitrite reductase as an ACE inhibitor.…”

Electroacupuncture improves cerebral blood flow and attenuates moderate ischemic injury via Angiotensin II its receptors-mediated mechanism in rats

“…The existence of brain renin-angiotensin system (RAS) has been reported previously, and it has been found to be involved in the modulation of cardiovascular and fluid-electrolyte homeostasis, as well as other brain-specific function. Evidence suggested that RAS blockade may have an impact on early mechanisms of vascular disease, such as endothelial dysfunction and vascular remodeling that underlie clinical manifestations of cardiovascular disease [ 6 ]. As a predominate bioactive peptide in RAS, Angiotensin II (AngII) has been suggested to be a significant contributor to the pathophysiology of ischemic stroke [ 7 – 9 ], which, after acting on its receptor (AngII type 1 receptor, AT 1 R; AngII type 2 receptor, AT 2 R ), can activate a series of cell signaling pathways, including phosphatidyl inositol (PI) signaling pathways that associated with vasoconstrictor function of Ang II.…”