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Endothelial‐dependent and –independent vasodilation in cerebral resistance arteries: Effects of age and estrogen Status
Author(s) -
McCroskey Casey,
Reyes Rafael Antonio,
LeBlanc Amanda Jo,
MullerDelp Judy
Publication year - 2007
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.21.6.a1238-d
Subject(s) - estrogen , vasodilation , medicine , endocrinology , cerebral arteries , ovariectomized rat , menopause , endothelial dysfunction , vascular resistance , nitric oxide , cardiology , hemodynamics
At menopause, women undergo an increase in risk for cardiovascular disease. Estrogen is known to play a role in modulating vascular function and providing protective cardiovascular effects. However, it is not known whether the protective cardiovascular effects of estrogen change with age. Therefore, the purpose of this study was to determine effects of age and estrogen status on endothelial‐dependent and –independent vasodilation in cerebral resistance arteries. Posterior communicating arteries (PCoA) were isolated from young (6 mo), middle aged (14 mo), and old (24 mo) in control (CON) and ovariectomized (OVEX) female Fischer‐344 rats, and flow‐, acetylcholine (ACh‐), and DEA‐NONOate–induced vasodilation were assessed. Flow‐induced vasodilation (FID) of the PCoA was preserved with age in intact female rats (6 mo: 73.9 ± 5.4 % vs. 24 mo: 82.4 ± 7.1%), but OVEX rats exhibited a lower FID in contrast to intact female rats (Ovex: 68.0 ± 4.1 % vs. CON: 79.8 ± 3.6%). Endothelium‐dependent dilation to ACh declined with age (6 mo: 51.3 ± 4.5%; 14 mo: 40.0 ± 5.9%; 24 mo: 33.2 ± 4.9%); however, ACh‐induced dilation increased in OVEX young rats (Ovex: 57.4 ± 6.9% vs. CON: 45.2 ± 5.9%). No age effect was present in DEA‐NONOate treated vessels. These data suggest both age and circulating ovarian hormones are determinants of vascular reactivity in cerebral resistance arteries and influence the risk for cerebral vascular disease. Funded by NIH grant HL077224.