Activation of human peripheral monocytes by angiotensin II

Abstract

This study has investigated the ability of the vasoconstrictor peptide angiotensin II to activate human peripheral blood monocytes. Activation was monitored by measuring both the release of tumor necrosis factor a from monocytes and their adhesion to monolayers of human endothelial cells. Angiotensin II-elicited activation of monocytes was dose-dependent (half-maximally effective concentration =0.2 nM), saturable (maximally effective concentration =5 nM), and sensitive to inhibition by the angiotensin type 1 receptor antagonist ZD 7155. Such direct actions imply that angiotensin II is an important candidate stimulus for the subendothelial infiltration of monocytes observed in atherogenesis and hypertension.

Oxidative stress is a critical mediator of the angiotensin II signal in human neutrophils: involvement of mitogen-activated protein kinase, calcineurin, and the transcription factor NF-κB

“…AT1 receptors for Ang II have been found recently in circulating neutrophils 4 and human peripheral monocytes, 5 and Ang II-induced cell activation in the latter has been reported. 6 In this context, the migration of leukocytes from blood to sites of inflammation and their adhesion to endothelial cells are primary events taking place during the acute inflammatory response and the pathogenesis of vascular diseases. 7 Because chronic inflammation of vessel walls is a hallmark of atherosclerosis, 8 and reactive oxygen species (ROS) such as superoxide anion (O 2 Ϫ ) and H 2 O 2 constitute the main intermediary molecules responsible for inflammation, 9 a link between atherosclerosis and ROS production has been postulated.…”

Angiotensin II Induces Leukocyte–Endothelial Cell Interactions In Vivo Via AT 1 and AT 2 Receptor–Mediated P-Selectin Upregulation

“…4 This may be directly relevant, because hypertension is associated with migration of monocytes through the vessel wall, a critical event leading to the development of the atherosclerotic lesion that can be attenuated by ACE inhibition. 5,6 Furthermore, Ang II can promote monocyte adhesion and activation in vitro [7][8][9] and stimulates the expression of monocyte chemoattractant protein-1 (MCP-1) and RANTES in several animal models in vivo. 5,10,11 In addition, Ang II releases a neutrophil chemoattractant factor from cultures of arterial endothelial cells.…”

Effects of ramipril in nondiabetic nephropathy: improved parameters of oxidatives stress and potential modulation of advanced glycation end products

“…Among the numerous factors shown to activate monocyte/macrophage function, AT II has been demonstrated to be an important mediator. 35,36 The unchanged or even slightly elevated neopterin levels during administration of ramipril suggest the role of AT II-independent factors. Interestingly, activation of monocytes/macrophages (as indicated by elevated neopterin, TNF-a and IL-1b levels) in heart failure was also uninfluenced by ACEI, even after administration of a high-dose regimen, reflecting a persistent immune activation by mechanisms other than AT II.…”