Presence of transendothelial channels in cerebral endothelium in chronic hypertension.

In this model hypertension developed as early as 1 wk. post-surgery and was associated with reduction in Ca2(+)-ATPase activity in cerebral vessels indicating that abnormalities in ionic calcium in vessel walls occur early in the evolution of hypertension. This study supports previous observations that cerebral cortical arterioles develop increased permeability to endogenous plasma proteins in chronic hypertension. The principal mechanism resulting in this increased permeability is enhanced pinocytosis. Ca2(+)-ATPase localisation in endothelial pinocytotic vesicles helped to localise transendothelial channels in occasional vessels of hypertensive rats. The latter findings reinforce the concept that in pathologic states associated with cerebral oedema, pinocytotic vesicles fuse to form transendothelial channels which transport plasma proteins into brain.