Arterial hypertension and its complications seem to be one of the most important current health problems. The heart is particularly exposed for the harmful influence of the chronically elevated blood pressure. Coronary atherosclerosis leading to ischaemic heart disease and myocardial infarction as well as left ventricular hypertrophy and heart failure are frequent consequences of arterial hypertension. However, in 15–20% of patients with hypertension and diagnosed ischaemic heart disease coronary angiography does not show any changes in coronary vessels. It is postulated that in this group of patients, myocardial perfusion defects resulted from coronary microcirculation disturbances are responsible for ischaemia. Vascular remodeling increases coronary resistance since it is associated with decrease in arteriolar lumen and eventually leads to the reduction of the density of arterioles and capillaries in the vascular bed (structural rarefaction) A second mechanism of hypertension causing myocardial ischaemia is related to left ventricular hypertrophy. Hypertrophied cardiomyocytes compressing coronary vessels decrease their vasodilating capacity. Increased left ventricular wall strain in arterial hypertension may also be involved in the process of impaired coronary reserve. There are several methods for coronary microcirculation assessment. Coronary flow reserve measurement during angiography is the invasive one. Among non invasive methods of coronary flow measurements echocardiographic techniques (both transesophageal and transthoracic), nuclear medicine techniques, positron emission tomography and cardiac magnetic resonance imaging should be mentioned. This article is a review of currently available methods for coronary microcirculation assessment. In the paper the results of different studies on myocardial perfusion in arterial hypertension are discussed. The article also brings up the problem of clinical meaning of disturbances in coronary microcirculation and possible therapeutic interventions by antihypertensive therapy improving coronary reserve.