Hypertension, otherwise known as high blood pressure, is a significant risk factor for the development and progression of atherosclerosis, the build-up of plaques within arteries, leading to blood vessel narrowing and stiffening. The connections between hypertension and atherosclerosis are complex and involves various mechanisms that contribute to vascular damage, inflammation, and plaque formation. High blood pressure firstly subjects endothelial cells lining the arterial walls to increased mechanical stress. Such stress can disrupt the integrity of the endothelial layer, compromising its function in regulating vascular tone, inflammation, and thrombosis. Endothelial dysfunction is a critical contributor to the initiation of atherosclerosis by promoting the subsequent adhesion of immune cells to the endothelium and facilitating the entry of lipids into the arterial wall. Hypertension also induces oxidative stress, characterized by an imbalance between the production of reactive oxygen species (ROS) and the body's antioxidant defence mechanisms. ROS damages cells within the vascular wall, including endothelial cells and smooth muscle cells (SMCs). Oxidized LDL cholesterol produced by increased cellular ROS is subsequently endocytosed or engulfed by macrophages, leading to the formation of foam cells, which are central contributors to early lesion development in atherosclerosis.Hypertension additionally triggers a chronic inflammatory response in the arterial wall. Inflammatory cytokines, such as interleukin-6 (IL-6) and tumour necrosis factor-alpha (TNF-α), are found to be elevated in hypertensive individuals. Inflammation in adipose tissue can lead to the secretion of IL-6 and TNF-α by adipocytes and immune cells residing in adipose tissue. Increased adipose tissue in obesity is known to significantly increase the risk of developing hypertension, with the prevalence of hypertension higher amongst individuals who are overweight or obese. These cytokines then attract immune cells to the vessel wall, leading to the recruitment of monocytes that then differentiate into macrophages which play a critical role in plaque formation by accumulating cholesterol and promoting inflammation within the lesions. Hypertension also leads to structural changes in blood vessels, including hypertrophy of smooth muscle cells and thickening of the arterial wall (vascular remodelling). Such remodelling can narrow the vessel lumen, reducing blood flow and creating a microenvironment conducive to atherosclerosis development by altering the balance of pro- and anti-inflammatory factors. The renin-angiotensin-aldosterone system (RAAS) is a hormonal system that regulates blood pressure. Angiotensin II, a key component of RAAS, is elevated in hypertension and promotes inflammation, oxidative stress, and vasoconstriction, contributing to the pathogenesis of atherosclerosis. Additionally, it can stimulate the migration and proliferation of smooth muscle cells, thereby contributing to the formation of fibrous caps in atherosclerotic lesions. Finally, hypertension is known to disrupt the normal flow patterns of blood (shear stress) within arteries. Such altered shear stress can impact endothelial function, plaque stability, and thrombosis risk. We provide a comprehensive product range of research reagents for investigating hypertension, including Integrin beta 3 antibodies, MRP1 antibodies, Urotensin II antibodies, Angiotensinogen ELISA Kits, and Cardiotrophin 1 ELISA Kits. Explore our full hypertension product range below and discover more, for less. Alternatively, you can explore our Vascular Remodelling, Vasoconstriction, and Sodium / Ion Transport product ranges.