Arterial hypertension is a major coronary risk factor due to an increase prevalence of coronary atherosclerosis. On the other hand, many arguments are suggestive of symptomatic or silent episodes of myocardial ischemia in hypertensive patients without coronary artery stenosis. Several pathophysiological processes that are implicated in coronary vascular changes are detrimental for the oxygen demand/supply equilibrium and adaptation of coronary circulation and coronary blood flow to an increase in myocardial oxygen demand. First, apart from coronary atherosclerosis, epicardial vessels are altered by vessel wall remodelling and structure changes. Second, structural alterations of the coronary arterioles due to medial hypertrophy and perivascular fibrosis limit the functional area of the vessels which are also compressed by a higher intramyocardial pressure, resulting in a reduction of coronary flow reserve. Third, the increase in intercapillary distance due to myocardial hypertrophy increases the distance of oxygen diffusion to cardiac myocyte mitochondria, the site of ATP synthesis. Fourth, the endothelium-dependent nitric-oxide dilation of coronary vessels is depressed, thus impairing the adaptation of coronary circulation to changes in myocardial oxygen demand. All these changes do not depend on myocardial hypertrophy, although myocardial hypertrophy aggravates the disorders. Antihypertensive therapy may have beneficial effects by reducing myocardial mass and arterial pressure, by restoring a normal vascular structure and architecture, and by improving coronary vasomotion.