Hypertension is a major factor for left ventricular hypertrophy, the development of ischemic heart disease and heart failure. Structural and functional alterations of the arteries and heart muscle plays a crucial role in development of these complications. Vascular damage in hypertension involves three interrelated mechanisms: pulsatile flow, endothelial cell changes and the remodeling and growth of smooth muscle cells. Vascular growth and remodeling may be induced by shear stress and mechanical stretch as well as by hormonal stimulation and growth factors. Alterations in structure and function of small vessels in hypertension include a smaller lumen which increases resistance to blood flow and an elevated media thickness to lumen ratio which may amplify responses to vasoconstrictors. The endothelium of these arteries has a reduced ability to induce vascular relaxation due to impaired structure and/or function. Impaired function of endothelium as well as hyperinsulinemia and dyslipidemia associated with hypertension promotes atherosclerosis. Changes in geometry and structure of large arteries decrease systemic compliance which may increase afterload. In hypertension left ventricular pressure overload that induces hypertrophy is caused by an increase in peripheral resistance, a decrease in aortic distensibility and early wave reflection from the periphery of the body. However not only hemodynamic factors but also neurohumoral stimulation and growth factors are involved in this process. Remodeling of the heart in hypertension involves myocytic hypertrophy, proliferation of fibroblasts with increased collagen content, interstitial fibrosis and remodeling ofcoronary arteries and arterioles. The structural vascular changes in hypertension may play an important role in the. progression of left ventricular dysfunction especially in the transitionofthe hypertrophic heart to the dilative and eccentric state and in the induction of cardiac failure by means ofthe chronic and progressive impairment of myocardial oxygen supply.