The question of whether influxes of ionic Ca+2 into cerebral endothelium plays an important role in increased vascular permeability consequent to an acute hypertension is not accurately resolved. We tested the effect of nifedipine, a calcium entry blocker, on the cerebrovascular permeability for proteins in adrenalin-induced acute hypertension. The experiments were carried out on male Wistar rats. The experimental groups consisted of normotensive saline controls, adrenaline-induced hypertensive rats, and adrenalin-induced hypertensive rats as pre-treated or post-treated with a bolus of nifedipine. Brains of hypertensive rats showed increased permeability to Evans Blue-Albumin complex, when blood pressure elevated rapidly to more than 170 mmHg. The number and size of areas of Evans-Blue extravasation were smaller if an increase in blood pressure was prevented. The short lasting elevation of blood pressure did not result in protein extravasation in brains of hypertensive rats. The results suggest that nifedipine can modify the permeability disruptions observed in acutely hypertensive rats. The data also support the hypothesis that Ca+2 may be responsible for the changes in permeability of BBB in hypertension by mediating the contraction of vascular muscles.