Intrauterine Growth Restriction Does not Change the Regulation of Arterial Contractile Responses in Rats during Early Postnatal PeriodстатьяИсследовательская статья
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Аннотация:Intrauterine growth restriction (IUGR) is one of the most common pathologies of pregnancy. Due to this pathology, the functioning of many systems, including the cardiovascular, is impaired. In adult animals, who have suffered IUGR, the contribution of procontractile mechanisms of vascular tone regulation (e.g., Rho-kinase signaling pathway) increases, while that of anticontractile mechanisms (e.g., endothelial NO), on the contrary, decreases, which can lead to vasospasm and impaired blood supply to the organs. Since NO and Rho-kinase play a pronounced vasomotor role in early postnatal ontogenesis, this work was aimed to assess the effect of IUGR on the contribution of these mechanisms to the regulation of arterial contractile responses during the early postnatal period in rats. IUGR was modeled by restricting the amount of food calories consumed by females (by 50%) since day 11 of pregnancy until parturition. In rat offspring aged 11–12 days, we studied the responses of the isolated saphenous artery in isometric mode and evaluated the content of mRNA and proteins of interest in this artery. IUGR did not alter the offspring arterial reactivity to the α1-adrenergic receptor agonist methoxamine. The increase in vasocontractile responses to methoxamine in the presence of the endothelial nitric oxide synthase (eNOS) inhibitor L-NNA, as well as the expression levels of eNOS (mRNA and protein) and arginase-2 (mRNA), did not change in the arteries of IUGR rat pups, whereas the arterial sensitivity to the exogenous NO donor DEA/NO was higher in IUGR vs. Control rat pups. Despite relatively low levels of RhoA and Rho-kinase II proteins in the arterial tissue of IUGR rat pups, the decrease in contractile responses, elicited by the Rho-kinase inhibitor Y27632, was equally pronounced in the arteries of rat pups from both IUGR and Control groups. Thus, IUGR, caused by maternal nutritional restriction during pregnancy, causes no pronounced changes in the regulation of systemic vascular tone during the early postnatal period.
