Cerebral endothelial plasma membrane alterations in acute hypertension

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Abstract
This study was undertaken to localize oligosaccharide residues on the endothelial luminal plasma membrane of cerebral vessels of normotensive animals and vessels permeable to horseradish peroxidase (HRP) in angiotensin-induced acute hypertension. Wistar-Furth rats were injected with HRP intravenously and hypertension was induced by an intravenous infusion of angiotensin amide. Animals were fixed 2.5, 10 and 15 min later and the HRP reaction product was demonstrated in brain slices, followed by lectin localization using the avidin-biotinperoxidase method. Oligosaccharide residues demonstrable on the luminal plasma membrane of cerebral endothelium of normotensive controls and both permeable and nonpermeable vessels of hypertensive animals were: α-d-mannosyl, α-d-glucosyl, β-N-acetylglucosaminyl, sialyl, β-d-galactosyl, α-l-fucosyl and α-N-acetyl-d-galactosaminyl groups. Peanut agglutinin did not bind to the endothelium of normotensive controls or of nonpermeable vessels in hypertensive animals, but did bind to endothelium of vessels permeable to HRP 2.5 min after the onset of hypertension. At 10 min, the luminal plasma membrane of vessels regained their normal characteristics and peanut agglutinin binding was no longer demonstrable. Our studies suggest that increased cerebrovascular permeability to protein in acute hypertension is associated with loss of the terminal sialic acid groups on the luminal plasma membrane of permeable vessels. This results in the observed reduction of charge on the endothelium and an exposure of β-d-gal-(1,3)-d-gal N-acetyl groups leads to binding of peanut agglutinin. Both alterations are rapidly reversible and no longer demonstrable 10 min after the onset of hypertension, when blood pressures reach resting levels and the blood-brain barrier is restored.