Hypertensive vascular disease and inflammation: mechanical and humoral mechanisms.
Clinical hypertensive vascular disease is the result of complex alterations in the biology of the cellular components of the arterial wall. In this review, the hypothesis will be put forth that elevated blood pressure induces an inflammatory state in the arterial wall through both humoral and mechanical signaling pathways. The generation of reactive oxygen species and subsequent upregulation of redox-sensitive proinflammatory gene products are common endpoints of these pathways. Subsequent adaptive and maladaptive responses of the wall occur as a result of the integration of the humoral and mechanical stimuli.
Taylor
W R
WR
Division of Cardiology, Department of Medicine, Atlanta VA Medical Center and Emory University School of Medicine, Atlanta GA 30322, USA.
D000818:Animals; D001161:Arteriosclerosis / Q000276:immunology*; D006439:Hemodynamics / Q000502:physiology; D006801:Humans; D006973:Hypertension / Q000276:immunology*; D018836:Inflammation Mediators / Q000097:blood*; D009131:Muscle, Smooth, Vascular / Q000276:immunology*; D015398:Signal Transduction / Q000502:physiology
D018836:Inflammation Mediators