Abstract

Our hypothesis is that hypoperfusion of the brainstem is due to elevated vertebrobasilar artery resistance, triggers hypertension. We asked: is there a functional relationship between the sympathetic innervation to the vertebrobasilar system and its remodelling in the SHR? SHRs (11–12 weeks old) received either sham surgery or bilateral SCGx. Animals recovered for 14 days, were then perfused-fixed with 4% PFA and the vertebrobasilar arteries examined using both immunohistofluorecent staining of sympathetic (anti-DβH) and parasympathetic (anti-VAChT) fibres, and by cross sectional examination of vertebral and basilar arteries. Bilateral SCGx reduced sympathetic innervation to all parts of basilar artery: anterior (SCGx 123 ± 35 vs sham 198 ± 77 fibres/mm2, p < 0.05), middle (86 ± 17 vs 204 ± 62 fibres/mm2, p < 0.001) and posterior (126 ± 29 vs 291 ± 73 fibres/mm2, p < 0.001) as well as both left (L) and right (R) vertebral arteries (VA, LVA 90 ± 33 vs 232 ± 67 fibres/mm2, p < 0.01 and RVA 88 ± 30 vs 238 ± 66 fibres/mm2, p < 0.01). The parasympathetic innervation to the vertebrobasilar arteries was unchanged after SCGx. Despite the reduction of sympathetic input there was no change to vertebrobasilar artery remodelling: the vessels’ external diameter, lumen size and wall thickness were unaffected by the SCGx. The SCG provides a major innervation to the vertebrobasilar arteries in the SHR but it is not the only source of sympathetic innervation. Reduction of sympathetic input to the vertebrobasilar arteries in SHR with established hypertension does not attenuate cerebrovascular remodelling at least over a 14 day period. Acknowledgements – Wellcome Trust, British Heart Foundation

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