Fig. 6

Converging mechanisms of cerebrovascular remodeling and microglia activation in chronic hypertensive states with BBB disruption and leukocyte infiltration into the CNS. (a) Identification of leukocyte recruitment into the hippocampus and cortex of all groups in early and late chronic hypertension, represented as the frequency of low FSC CD45.⁺ events from the total single live cells. (b) phase-contrast image of isolated microvessel derived from brain cortices plated on a microscope slide (scale bar, 50 µm). Quantification changes in gene expression in cerebral microvessels of tight junction genes (c) Cldn5, Ocln, and adhesion molecules Icam1 and Vcam1 (d) at early and late chronic hypertension shown by qRT-PCR. In normotensive and hypertensive rat brains. Fold changes were calculated by normalizing gene expression levels to GAPDH. The resulting data were further normalized on mean values of normotensive controls. (e) Representative IgG Fluorescence in cortical brain sections (f)% of IgG examined per FOV. Bar graphs represent mean ± SEM. Claudin 5; Ocln, occludin; Icam1, intercellular adhesion molecule-1; Vcam1, vascular cell adhesion molecule-1;FOV, field of view; IgG, immunoglobulin G. p-values: * ≤ 0.05; ** for p ≤ 0.01; *** for p ≤ 0.001; **** for p ≤ 0.0001