Arterial hypertension (AH) is the major independent risk factor for cardiovascular and cerebrovascular morbidity and mortality. Success in treatment of hypertonic patients is currently still far from acceptable in developing countries but also in the most of the developed countries in the world. There are numerous reasons and explanations for such poor therapeutic outcome, with poor patient's awareness of the need to pay attention to his own health and occasional superficial physician's approach being only some of them. However, AH treatment may present as an exceptional problem in some patients. Despite sufficient therapy duration and optimal doses of three types of antihypertensives, including one diuretic, no decrease in arterial blood pressure was observed in a low number of patients, so that such AH is called refractory (RH). RH may be primary if present since the beginning of treatment, or secondary if presenting after a period of successful treatment. In case of secondary RH, secondary forms of AH should be considered, like renovascular hypertension, primary aldosteronism, etc. In cases of primary RH, it is necessary to exclude pseudohypertension, pseudoresistance and pseudotolerance before characterizing a patient as really resistant, when the cause should be primarily sought in pathomechanisms of those organ systems which otherwise play an important role in AT homeostasis or in etiopathogenesis of AH, i.e. in kidney and heart. A significant reason for refractoriness may be drug interactions or applications of hypertensives which are not an optimal choice according to hemodynamic or hormone background of increased blood pressure. Clearly, it is not always easy to determine the background of refractoriness in practice, yet fortunately such patients are not frequent and additional efforts dedicated to them are not at the time needed for other patients. In this paper we presented a review of the most frequent causes of refractoriness in AH treatment, possible errors in diagnosing RH, and pathomechanisms responsible for the occurrence of resistance. Prognosis of RH is considerably worse than in otheR hypertonic patients and, since the possibilities of treatment are not extensive, a review of possible therapeutic approaches is also presented depending on the pathogenetic background of resistance. As RH patients have increased body mass index, and the success of the therapy was observed to depend on the salt intake, particular attention should be paid to instructions for patients on the change in lifestyle. The treatment of RH patients is a serious challenge which may unfortunately be frustrating and not infrequently have a fatal outcome due to either disease progression or patient's obstinacy.