Hypertension and the blood-brain barrier.
Acute hypertension leads to alternating regions of dilation and vasoconstriction of surface cerebral vessels. It remains to be determined conclusively if either or both of those calibre changes are essential in the production of degenerative vascular changes of malignant hypertension. There is no evidence of ischemic or other morphologic change to components of the blood-brain barrier including the interendothelial tight junctions which remain intact. An early phase of evolving cerebral edema is swelling of astrocytic foot processes that occurs only in regions of abnormal protein permeability. The cortical location of these acute hypertensive lesions stands in contrast to the ganglionic location of the microaneurysms found as complication of chronic hypertension in man. The location of permeability changes to protein do not necessarily reflect changes in brain water permeability susceptible to sympathetic regulation.
D000208:Acute Disease; D000818:Animals; D001812:Blood-Brain Barrier; D001929:Brain Edema / Q000503:physiopathology*; D002199:Capillary Permeability; D002536:Cerebral Arteries / Q000503:physiopathology*; D002560:Cerebrovascular Circulation; D006735:Horseradish Peroxidase; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D051381:Rats; D013045:Species Specificity; D014661:Vasoconstriction; D014664:Vasodilation
D006735:Horseradish Peroxidase