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Glucosamine chronic treatment differently modulates uterine artery from pregnant and virgin Wistar rats
Author(s) -
Justina Vanessa Dela,
Webb R Clinton,
Lima Victor Vitorino,
Giachini Fernanda Regina
Publication year - 2019
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.2019.33.1_supplement.lb595
Subject(s) - glucosamine , enos , endocrinology , medicine , uterine artery , endothelial dysfunction , endothelium , phenylephrine , acetylcholine , pregnancy , vasodilation , chemistry , western blot , nitric oxide , nitric oxide synthase , gestation , biology , biochemistry , blood pressure , genetics , gene
Background O‐linked β‐N‐acetylglucosamine (O‐GlcNAc) is a post‐translational modification that modulates several proteins related to the vascular tone control. Dysregulation of O‐GlcNAcylation occurs in a wide range of diseases, favoring endothelial dysfunction. During pregnancy, vascular dysfunction observed in the uterine vasculature results in inadequate nutritional support between the maternal‐fetal interface. It remains to be elucidated whether augmented O ‐GlcNAc levels impact uterine artery (UA) function from virgin or pregnant rats. Hypothesis Increased O ‐GlcNAc impairs the endothelial function of the uterine artery. Methods Pregnant or virgin Wistar rats (14‐week old) were treated either with glucosamine (300 mg/Kg) or vehicle, for 21 days, i.p. The UAs were rapidly removed, cleaned from fat tissue and mounted for isometric force development record. Concentration response‐curves to acetylcholine (1 nM to 100 μM) were performed in UA contracted with phenylephrine (10 μM), in the presence or absence of L‐NAME (100 μM, 30 minutes). Protein expression was evaluated by western blot. Results Glucosamine treatment increased O ‐GlcNAc expression in UAs from virgin rats (p= 0.04). Decreased endothelium‐dependent relaxation was observed in UAs from treated virgin rats compared to vehicle [Emax 56.16 ± 4.18 vs. 76.38 ± 3.92%, respectively], which was abolished by incubation with L‐NAME. Endothelial nitric oxide synthase (eNOS) activity was decreased (p=0.04) by glucosamine‐treatment in virgin rats. On the other hand, in pregnancy, treatment with glucosamine decreased O ‐GlcNAc expression (p=0.03) in UAs compared to vehicle. Increased sensitivity to acetylcholine [pD 2 6.43 ± 0.13 vs. 6.90 ± 0.11] was observed in the UAs of glucosamine‐treated pregnant rats compared to vehicle pregnant rats with no differences in the maximal response. eNOS activity was unchanged between these groups. Conclusions Glucosamine‐treatment impairs UA endothelial function in virgin, but not in pregnant rats. Support or Funding Information CAPES FAPEG NIH (HL‐134604) This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .