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The effects of chronic estrogen supplementation on neuropeptide Y neurotransmission in skeletal muscle arterioles
Author(s) -
Evanson Kirk W,
Stone Audrey J,
Kluess Heidi A
Publication year - 2011
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.25.1_supplement.1026.28
Subject(s) - medicine , endocrinology , neuropeptide y receptor , estrogen , vasoconstriction , chemistry , neuropeptide , receptor
The purpose of this study was to determine the effects of chronic estrogen supplementation on NPY neurotransmission in gastrocnemius first‐order arterioles (G1A) of adult female rats. Female rats (4 mo; n = 30) were ovariectomized (OVX) with a subset (n = 15) receiving an estrogen pellet (OVE; 17β‐estradiol (4μg/day)). Red G1A were excised and cannulated with micropipettes connected to albumin reservoirs. NPY‐mediated vasoconstriction via a Y 1 ‐agonist decreased vessel diameter 59.74 ± 3.80% as compared to baseline; however, there were no group differences in EC50 (OVE: −8.97 ± 0.36; OVX: −8.72 ± 0.20 log M [Leu31Pro34]NPY) or slope (OVE: −1.37 ± 0.38; OVX: −1.64 ± 0.31 % baseline/log M [Leu31Pro34]NPY). NPY overflow experienced a slight increase following field stimulation, and significantly increased (p < 0.05) over control conditions in the presence of a DPPIV inhibitor (diprotin A). These data suggest that NPY can induce an estrogen‐independent decrease in vessel diameter in G1A, and DPPIV is active in mitigating NPY overflow in adult female rats. This research was supported by the Arkansas Biosciences Institute and the NIA (grant no. 5R03AG033245).