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Endothelium‐dependent vasodilation in cerebral resistance arteries: effects of age and estrogen status (680.8)
Author(s) -
Kilar Cody,
Reyes Rafael,
Kang Lori,
LeBlanc Amanda,
McCroskey Casey,
Bryan Robert,
MullerDelp Judy
Publication year - 2014
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.28.1_supplement.680.8
Subject(s) - estrogen , ovariectomized rat , medicine , endocrinology , nitric oxide , chemistry
Postmenopausal women have increased risk of cerebrovascular disease, possibly related to loss of cardioprotective estrogen. We investigated the effects of age and estrogen status on flow‐induced dilation (FID) and the role of nitric oxide (NO) in FID of cerebral resistance arteries. Young (Y), middle‐aged (MA) and old (O) female rats were placed in the following groups: intact, ovariectomized (ovex) and ovariectomized with estrogen replacement (ovex +E). FID was assessed in posterior communicating arteries (PCoA) with and without L‐NAME to block NO synthase. FID declined with age in PCoA of intact rats. Ovex reduced FID in PCoA of Y and MA rats, but not in PCoA of O rats. Ovex +E restored FID in Y rats but decreased FID in O rats. L‐NAME reduced FID in PCoA of intact Y and MA rats, but not in PCoA of intact O rats. In contrast, L‐NAME reduced FID in MA and O ovex rats, but did not affect PCoA of Y ovex rats. In ovex + E groups, L‐NAME inhibited FID in PCoA of Y rats, but did not alter FID in PCoA of MA or O rats. Thus, NO contributes to FID in PCoA of both Y and MA, but not O intact rats. Estrogen removal eliminates NO‐mediated FID in PCoA of Y rats, but upregulates NO signaling in PCoA of O rats. Estrogen replacement restores FID in PCoA of Y rats, but exacerbates declining FID in PCoA of O rats. Age‐related loss of ovarian estrogen contributes to impairment of NO‐mediated FID in PCoA; however, exogenous estrogen cannot restore NO‐mediated FID in old PCoA.