Cardiac constituents affected in arterial hypertension comprise the myocardium, interstitium and coronary circulation. With regard to coronary circulation, arterial hypertension is an important risk factor in coronary artery disease, but even in the absence of coronary artery disease, hypertensive patients frequently have angina pectoris or reveal electrocardiographic abnormalities suggestive of myocardial ischaemia due to coronary insufficiency. Under clinical conditions, determination of coronary flow reserve (dipyridamole; Argon-method) allows for the evaluation of impairment of coronary regulatory reserve. In comparison to healthy normotensives, coronary haemodynamics in hypertensive patients with microvascular angina are characterized by a severely increased minimal coronary resistance and reduced maxmial coronary blood flow to dipyridamole. Accordingly, coronary reserve is markedly reduced by about 40%, and metabolic, myocardial and vascular factors may be involved in this reduction. In the compensated stage of arterial hypertension, with concentric left ventricular hypertrophy, myocardial factors, such as myocyte hypertrophy, extravascular compressing forces and functional implications of impaired relaxation, as well as metabolic factors, contribute to impairment in coronary reserve to a minor extent. The reduction in coronary flow reserve is not proportional to the elevation in left ventricular muscle mass and thus the degree of left ventricular hypertrophy does not seem to determine the reduction in vasodilator reserve directly. Thus the reduction in coronary reserve seems to be primarily the consequence of an impaired vasodilating capacity of the coronary resistance vessels, as indicated by a severely increased minimum coronary resistance to dipyridamole, i.e. a severely reduced overall coronary conductance capacity. Structural changes of the small coronary resistance vessels, such as medial thickening and perivascular fibrosis, might therefore play a key role in the pathophysiological-anatomical background of the impaired coronary reserve. With the occurrence of chamber enlargement, increased systolic wall stress may also restrict coronary reserve metabolically, and increased diastolic wall stress by an increment in extravascular compressive force. Finally, at the coronary microcirculation level coronary insufficiency in hypertensive patients with angina pectoris and normal coronary angiogram may also be due to impairment of the endothelium-dependent vasodilation of the small resistance vessels.