Impact of Normal and Overweight Pregnancy in GLUT4 and Glucose-Dependent Vascular Contractility

Abstract

<b><i>Introduction:</i></b> Obesity during pregnancy can contribute to hypertensive complications through changes in glucose utilization. We investigated the impact of vascular glucose uptake, GLUT4 density, and endothelium on agonist-induced vasoconstriction in the aortas of overweight pregnant rats. <b><i>Methods:</i></b> Isolated aortic rings with or without endothelium from pregnant or nonpregnant rats fed a standard (SD) or hypercaloric diet (HD) were contracted with phenylephrine or serotonin (10⁻⁹ to 10⁻⁴<sc>M</sc>) using standard (11 m<sc>m</sc>) or without (0 m<sc>m</sc>) glucose Krebs solution. GLUT4 density in the aortas was measured using the en face method. <b><i>Results:</i></b> Aortas from overweight pregnant animals (PHD) showed increased Phe-induced vasoconstriction (<i>p</i> &lt; 0.05 vs. pregnant standard diet [PSD]), which was endothelium-independent. The contraction decreased significantly in the absence of glucose. In contrast, vessels from pregnant SD rats maintained their contraction in glucose-free Krebs solution. 5-HT increases PHD aortic contraction only in the absence of glucose. The fetal aortas from PHD mothers showed blunted vasoconstriction. Overweight significantly reduced GLUT4 expression in maternal and fetal aortas (<i>p</i> &lt; 0.05 vs. PSD). <b><i>Conclusions:</i></b> Aortic contractility is independent of glucose uptake during healthy pregnancy. In contrast, overweight pregnancy increases contractility. This increase depends directly on smooth muscle glucose uptake and inversely on GLUT-4 density. The increased contraction observed in the vasculature of overweight mothers was inverted in the fetal aortas.