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Maternal vasculature changes produced by experimental gestational diabetes mellitus by obesity (1051.10)
Author(s) -
Tufiño Cecilia,
Rosas Paula,
Bobadilla Rosa
Publication year - 2014
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.28.1_supplement.1051.10
Subject(s) - losartan , medicine , endocrinology , gestational diabetes , angiotensin ii , angiotensin ii receptor type 1 , diabetes mellitus , offspring , phenylephrine , telmisartan , obesity , renin–angiotensin system , vasoconstriction , gestation , receptor , pregnancy , biology , blood pressure , genetics
Gestational diabetes mellitus is an increasing incidence disease whose short‐term consequences in the maternal vasculature are poorly understood. The purpose of this study was to determine whether an experimental model of obesity induced gestational diabetes mellitus can modify the vasoconstrictor response of isolated arteries and if so, to explore the possible causes. Wistar rats were subjected to a high calorie diet for 7 weeks, of which the last three coincided with the period of gestation. GDM was defined by an abnormal glucose tolerance test. GDM group was compared with a control, obese, and healthy pregnant group. Dose response curves to phenylephrine and angiotensin II were done in isolated aortic rings. Also, plasma levels of angiotensin II and expression of the COX‐1, COX‐2, iNOS and AT1 receptors for angiotensin II were measured. Results showed that GDM group presented impaired glucose tolerance and an increase in the vasoconstrictor response in the presence of losartan or prazosin associated with an increase in the protein expression of AT‐1 receptor, COX‐2 and iNOS. These results provide evidence that obesity occurs DMG deleterious changes in the short‐term maternal vasculature.