Hypertension is generally considered the most important treatable factor for stroke. The relative risk of stroke among hypertensive persons, is approximately threefold to tenfold greater than for nonhypertensive persons, and even borderline hypertension is associated with a relative stroke risk that is about three times that of normotensine persons. In most studies, increased diastolic blood pressure (BP) has emerged as an independent risk factor responsible for up to 70% of strokes. The risk of stroke increases in an exponential manner as diastolic BP increases throughout the range of 70-110 mm Hg. A 7,5 mm Hg rise in diastolic BP is associated with a doubling of stroke risk. Cerebral blood flow is regulated by changes of vascular resistance. Resistance can be modulated by local-chemical and endothelial factors as H+, K+, Ca++ ions, adenosine, and osmolarity. Endothelial factors such as thromboxane A2 endothelin derived constrictor factor, autacoids like histamine, bradykinin, and free radicals also influence cerebrovascular resistance. Cerebral autoregulation may be partly or completely lost after stroke. Structural adaptation of the vasculai wall to longstanding hypertension, such as hypertrophy of smooth muscle and proliferation of connective tissue, may play an important role in reducing cerebral blood flow (CBF). Local arteriolopath-lipohyalinosis of small penetrating artery and narrowing of large extra- and inctracranial arteries has been suggested to result from chronic hypertension. Hypertensive individual have reduced hemodynamic reserve and are more susceptible to cerebral ishaemia. In chronic hypertension CBF autoregulation is adapted to high BP: the lower end of autoregulation curve is shifted towards high pressure. The risk of provoking cerebral ischaemia by antihypertensive treatment is possible in a/ initial treatment of patients with accelerated hypertension, b/ in the elderly hypertensive, c/ in patients with transient cerebral symptoms, d/ in acute stroke patients with transient hypertension.