Efeitos da exposição pré-natal ao álcool na expressão de peptídeos vasoativos dos sistemas renina-angiotensina e calicreína-cininas no hipocampo de camundongos

Abstract

Prenatal exposure to alcohol (PAE) impairs fetal development and can result in neuronal inflammation and death in the Central Nervous System (CNS). Thus, it can contribute to phenotypes of neurological disorders and changes in behavior, memory, and learning. These latter changes are controlled by the hippocampus. Hippocampal expression of components of the Renin-Angiotensin (RAS) and Kallikrein-kinin (KKS) peptide systems has already been described, however, a possible modulation generated by alcohol of these systems in PAE is still unknown. This exploratory study analyzed the effects of PAE on the expression of the RAS and KKS peptide systems in the hippocampus of mice of both sexes. Thus, isogenic C57Bl/6 mice were exposed to alcohol during pregnancy at a concentration of 10% (v/v). On a postnatal day 45 (PN45), mouse hippocampi were processed for differential analysis of messenger RNA (mRNA) expression of components of the RAS and KKS systems. In addition to the difference in baseline mRNA expression of RAS peptides between genders (control group), PAE modulated mRNA expression of components of both systems in males and females, evidencing a possible protective role against damage caused by alcohol in the hippocampus. The high expression of AT1 and ACE mRNA in males and a possible RAS modulation by estrogen suggest that females from the PAE group may be protected by the effect of alcohol. The use of drugs that regulate these systems may be a strategy to reduce the effects of PAE on the hippocampus.