Association between the Molecular Pathobiology of Essential Hypertension and Thrombotic Diseases
Abstract
From the Departments of Immunology and Vascular Biology, The Scripps Research Institute, La Jolla, California The clinical association of hypertension and heart disease has been recognized for more than a century. However, a direct association between hypertension and thrombosis is not apparent. With the introduction of therapeutic interventional coronary artery ballooning and related procedures including introduction of stents, the occurrence of secondary local vasculopathy as well as thrombosis presents a significant threat. The view that hypertension, which is mediated by angiotensin II, is the immediate driving force for the various forms of associated vasculopathy is naive. Angiotensin II is the product of the renin, angiotensinogen, angiotensin-converting enzyme cascade. Recent studies have identified the cellular effects of angiotensin II as highly pleomorphic. 1 Apart from the well recognized effects of angiotensin II on local vascular tension, namely vascular smooth muscle contraction, it is now recognized that angiotensin II, via engagement of its cognate endothelial surface receptor AT 1 , induces biosynthesis and local release of a number of cell modulatory proteins including platelet-derived growth factor, basic fibroblast growth factor, insulin growth factor, transforming growth factor-ß, and undoubtedly other molecules, as well as molecules influencing the thrombogenic pathways, such as