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Hypertension‐induced endothelial dysfunction and posterior communicating artery remodeling
Author(s) -
Pires Paulo Wagner,
Dorrance Anne McLaren
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.700.3
Subject(s) - medicine , circle of willis , endothelial dysfunction , cardiology , lumen (anatomy) , basilar artery , posterior communicating artery , posterior cerebral artery , cerebral arteries , occlusion , middle cerebral artery , perfusion , ischemia , internal carotid artery
Hypertension‐induced endothelial dysfunction and remodeling of arteries in the circle of Willis can impair blood flow after permanent middle cerebral artery (MCA) occlusion. The posterior communicating artery (PComA) connects the basilar and posterior cerebral artery (PCA). The PCA forms anastomoses with the MCA, thus flow through the PComA/PCA can improve perfusion of the MCA territory. The effects of hypertension on PComAs are unknown; we hypothesized that hypertension will lead to inward remodeling and endothelial dysfunction. PComAs from adult male stroke‐prone spontaneously hypertensive rats (SHRSP, n=3) were studied using pressure myography. Wistar‐Kyoto (WKY) rats were controls (n=5). Data are means±SEM, SHRSP vs WKY rats. Dilation to 2‐methylthio‐ATP was impaired in SHRSP (change in diameter at 10μM: 17.6±6 vs 24.5±3μm, p<0.05). At 80mmHg, the lumen diameter (172±17 vs 205±17μm, p<0.05) and distensibility (49±6 vs 61±5%, p<0.05) of PComAs from SHRSP were reduced and the wall thickness (15±1 vs 12±1, p<0.05) and wall/lumen ratio (0.09±0.01 vs 0.06±0.01, p<0.05) were increased. These data suggest that hypertension causes endothelial dysfunction and inward remodeling of the PComA and this may reduce collateral blood flow after permanent cerebral ischemia.