Influence of estradiol supplementation on neuropeptide Y neurotransmission in skeletal muscle arterioles of F344 rats
Influence of estradiol supplementation on neuropeptide Y neurotransmission in skeletal muscle arterioles of F344 rats
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DOI：
10.1152/ajpregu.00072.2012
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发表时间：
2012-09-01
影响因子：
2.8
通讯作者：
Kluess, Heidi A.
中科院分区：
文献类型：
--
作者：
Evanson, Kirk W.;Stone, Audrey J.;Kluess, Heidi A.
埃文森 KW、斯通 AJ、萨姆拉吉 E、本森 T、普里斯比 R、克鲁斯 HA。补充雌二醇对 F344 大鼠骨骼肌小动脉神经肽 Y 神经传递的影响。 Am J Physiol Regul Integr Comp Physiol 303：R651-R657，2012。首次发表于 2012 年 7 月 25 日； doi: 10.1152/ajpregu.00072.2012.-尚未描述雌二醇对骨骼肌阻力血管中神经肽 Y (NPY) 神经传递的影响。本研究的目的是确定长期补充雌二醇对成年雌性大鼠腓肠肌一级小动脉 NPY 溢出、降解和血管收缩的影响。雌性大鼠（4 个月；n = 34）被切除卵巢（OVX），其中一部分（n = 17）接受雌二醇颗粒（OVE；17 β-雌二醇，4 μg/天）。治疗阶段（8周）结束后，切除小动脉，置于生理盐水溶液（PSS）浴中，并用连接至白蛋白储存器的微量移液器插管。与基线相比，通过 Y-1 激动剂 [Leu31Pro34]NPY 介导的血管收缩使血管直径减少 44.54 +/- 3.95%；然而，EC50（OVE：-8.75 +/- 0.18；OVX：-8.63 +/- 0.10 log M [Leu31Pro34]NPY）或斜率（OVE：-1.11 +/- 0.25；OVX：-1.65 +/- 0.34% 基线/log M [Leu31Pro34]NPY）没有组间差异。 NPY 不会增强去甲肾上腺素介导的血管收缩作用。 NPY 溢出在场刺激后略有增加，并且在 DPPIV 抑制剂（二蛋白 A）存在的情况下比对照条件显着增加（P < 0.05）。雌二醇状态不影响 DPPIV 活性。这些数据表明，NPY 可以诱导骨骼肌一级小动脉的血管直径适度减小，并且 DPPIV 可以有效减轻年轻成年雌性大鼠的 NPY 溢出。长期补充雌二醇不影响 NPY 血管收缩、溢出或其在骨骼肌一级小动脉中的酶分解。
Evanson KW, Stone AJ, Samraj E, Benson T, Prisby R, Kluess HA. Influence of estradiol supplementation on neuropeptide Y neurotransmission in skeletal muscle arterioles of F344 rats. Am J Physiol Regul Integr Comp Physiol 303: R651-R657, 2012. First published July 25, 2012; doi: 10.1152/ajpregu.00072.2012.-The effects of estradiol on neuropeptide Y (NPY) neurotransmission in skeletal muscle resistance vessels have not been described. The purpose of this study was to determine the effects of long-term estradiol supplementation on NPY overflow, degradation, and vasoconstriction in gastrocnemius first-order arterioles of adult female rats. Female rats (4 mo; n = 34) were ovariectomized (OVX) with a subset (n = 17) receiving an estradiol pellet (OVE; 17 beta-estradiol, 4 mu g/day). After conclusion of the treatment phase (8 wk), arterioles were excised, placed in a physiological saline solution (PSS) bath, and cannulated with micropipettes connected to albumin reservoirs. NPY-mediated vasoconstriction via a Y-1-agonist [Leu31Pro34]NPY decreased vessel diameter 44.54 +/- 3.95% compared with baseline; however, there were no group differences in EC50 (OVE: -8.75 +/- 0.18; OVX: -8.63 +/- 0.10 log M [Leu31Pro34]NPY) or slope (OVE: -1.11 +/- 0.25; OVX: -1.65 +/- 0.34% baseline/log M [Leu31Pro34]NPY). NPY did not potentiate norepinephrine-mediated vasoconstriction. 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). Estradiol status did not affect DPPIV activity. These data suggest that NPY can induce a moderate decrease in vessel diameter in skeletal muscle first-order arterioles, and DPPIV is active in mitigating NPY overflow in young adult female rats. Long-term estradiol supplementation did not influence NPY vasoconstriction, overflow, or its enzymatic breakdown in skeletal muscle first-order arterioles.