ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2012
Influence of estradiol supplementation on neuropeptide Y neurotransmission in skeletal muscle arterioles of F344 rats.
Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 11 citations in OpenAlex.
- Dipeptidyl Peptidase IV as a Muscle Myokine.Frontiers in physiology · 2020Review
- Endogenous dipeptidyl peptidase IV modulates skeletal muscle arteriolar diameter in rats.Physiological reports · 2018Article
- In vivo transplantation of 3D encapsulated ovarian constructs in rats corrects abnormalities of ovarian failure.Nature communications · 2017Article
- From one generation to the next: a comprehensive account of sympathetic receptor control in branching arteriolar trees.The Journal of physiology · 2015Article
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Authors and funding
6 authors at 4 institutions in 1 country.
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Abstract
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; 17β-estradiol, 4 μg/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 EC(50) (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.
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