Abstract
Experimentally induced acute angiotensin hypertension increases the permeability of cerebral arterioles, venules and veins to plasma components within a few hours. This increase in permeability was demonstrated by means of circulating homologous fluorescent serum proteins and colloidal carbon particles. An increased permeability of the cerebral vessels to plasma components is either a causal or an additional pathogenetic factor in the development of hypertensive encephalopathy.