Abstract
The vessel wall tension is the product of pressure and internal radius divided by the vessel wall thickness. Hence, dilated vessels will be exposed to higher tension at a given intraluminal pressure. Provided the rise in cerebrovascular intraluminal pressure is sufficiently prominent, transient opening of the morphologic blood-brain barrier will occur. In the present study pressure increase, not sufficient in itself to cause barrier opening, was induced. However, at concomitant dilatation of the vessels – as induced by CO2 or papaverine – under otherwise identical pressure conditions a barrier opening was obtained. Hence, vasodilatation of cerebral vessels will increase their vulnerability to hypertension.