In atherosclerosis numerous qualitative and quantitative changes in connective tissue metabolism parameters in serum and aorta occur. The elastin turnover is accelerated due to increased activity of elastases in serum and arterial wall. The activity of protease inhibitors is decreased. Also, the collagen's content of arterial wall was shown to be higher. Connective tissue is an important factor in regulation of smooth muscle cells (SMC) proliferation and migration, immunological processes during atherosclerosis and interactions with blond cells. The renin-angiotensin system plays an important role in atherogenesis and hypertension. Angiotensin II (ANG II) was shown to stimulate the phenotypic modulation of SMC. It induces SMC proliferation and migration from media to subendothelial layer, enhances the action of other growth factors, induces the adhesion and migration of monocytes and macrophages roto vascular wali, activates platelets and reduces fibrinolytic activity, stimulates modifications ofLDL particles and foam cells accumulation. During vascular injury there is an enhanced activity oflocal reninangiotensin system. It leads to overproduction of ANG II, both in serum and arterial wali. ANG II stimulates SMC to oversynthesize the extracellular matrix components - collagens type I and III, fibronectin, tenascin, thrombospondin, osteopontin and glycosaminoglycans - chondroitin and dermatan sulfates. It was shown that SMC under influence of ANG II synthesize less elastin.