Arterial hypertension is a serious and common complication of cyclosporine administration in humans. The prevalence of arterial hypertension in patients following orthotopic heart transplantation ranges from 38% to 92%. There are several characteristic features of this form of hypertension, including very early onset--usually within 4 to 6 weeks after transplantation and persistence with little alteration overtime. Diurnal profile shows the lack of normal nocturnal decline in blood pressure (BP) and appearance of the highest values of BP early in the morning. This phenomenon is caused by altered regulation of BP due to cardiac denervation. There was shown no correlation between the dose of cyclosporine and development of posttransplant arterial hypertension. It develops also independently of many investigated pretransplant and posttransplant cardiovascular risk factors. A great deal of attention has been focused on explantation of cyclosporine influence leading to hypertension occurrence. suggested mechanisms of this action are: elevation of systemic vascular resistance, prostaglandines and tromboxance production imbalance, hypomagnesemia, increased intravascular volume, modulation of sympathetic activity, nephrotoxicity. Reninangiotensin system seems to be not significantly associated with posttransplant hypertension, whereas the role of corticosteroides is still controversal. Hypertension remains the most common complication associated with cyclosporine administration in heart transplant recipients. Mechanisms of cyclosporine action leading to development of hypertension are still unknown. Further investigation is also needed into clinical significance of posttransplant hypertension and its influence on long-term survival after heart transplantation as they remain undefined.