Sympathetic nerves protect against blood-brain barrier disruption in the spontaneously hypertensive rat.

Abstract

SUMMARY The cerebral vessels of spontaneously hypertensive rats (SHR) are reported to have an in­ creased luminal size and decreased wall thickness after chronic sympathetic denervation. In order to evaluate a possible physiological significance of this observation, we studied blood-brain barrier protein transfer in two month old SHR and their normotensive controls, Wistar-Kyoto (WKY), during profound vasodilation stimuli one month after a unilateral superior cervical ganglionectomy. Our hypothesis was that during acute vaso­ dilation, protein transfer, which is dependent on vessel tension (tension = pressure X radius/wall thickness), would be greater in the vasculature of the chronically denervated (De) than in contralateral innervated hemi­ sphere (In). Vasodilation was induced with acute hypertension (norepinephrine) and seizures (bicucilline). Immediately prior, the cervical trunk to the innervated hemisphere was sectioned to prevent acute sympathetic neuronal effects. Protein transfer was assessed qualitatively with Evans blue dye and quantitatively with radio­ iodinated albumin. Successful chronic denervation was demonstrated by the absence of histofluorescence in De. Evans blue dye staining of SHR (n = 3) cerebral hemispheres was greater in De than in In. Radioiodinated albumin protein transfer was elevated in SHR De compared to In in each of eight animals studied (De-In = 0.16 ± 0.04%*, *p < 0.01); WKY (n = 8) De protein transfer was not different from In (De-In = 0.07 ± 0.05%). These results suggest that the trophic influence of sympathetic nerves on SHR cerebral vessels con­ tributes to protection of the blood-brain barrier during hypertension and seizures.