Date of Graduation


Document Type


Degree Name

Doctor of Philosophy in Kinesiology (PhD)

Degree Level



Health, Human Performance and Recreation


Heidi A. Kluess

Committee Member

Dean R. Gorman

Second Committee Member

David L. Kreider

Third Committee Member

Sean W. Mulvenon

Fourth Committee Member

Charles E. Riggs


Biological sciences, Arterioles, Dipeptidyl peptidase, Estrogens, Neuropeptide Y, Skeletal muscle


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)). Following conclusion of the treatment phase (8 weeks), red G1A were excised, placed in a physiological saline solution (PSS) bath, and cannulated with micropipettes connected to albumin reservoirs. A sampling port was placed immediately below the vessel to assess NPY overflow. The contralateral red G1A was homogenized in PSS for dipeptidyl peptidase IV (DPPIV) assay. NPY-mediated vasoconstriction via a Y1-agonist, [Leu31Pro34]NPY, decreased vessel diameter 44.54 ± 3.95% 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 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). Estrogen status did not affect DPPIV activity. These data suggest that NPY can induce a moderate decrease in vessel diameter in skeletal muscle G1A, and DPPIV is active in mitigating NPY overflow in young adult female rats. Chronic estrogen supplementation did not influence NPY vasoconstriction, overflow, or its enzymatic breakdown in skeletal muscle G1A.

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Endocrinology Commons