FUNCTIONAL VASCULAR PROGRAMMING IN YOUNG RATS: CONSEQUENCES OF EXPOSURE TO REPEATED MATERNAL IMMOBILIZATION STRESS DURING LATE GESTATION

Resumo

Prenatal exposure to chronic gestational stress provides a valuable experimental framework for examining early transgenerational effects, including significant repercussions on the cardiovascular system of the young offspring. Particular attention has been directed toward the modulation of catecholamine-mediated vasoconstriction and endothelium-dependent relaxation prior to the emergence of compensatory mechanisms in adulthood or the development of overt structural alterations. The present study aimed to investigate the effects of repeated (chronic) maternal immobilization stress during late gestation (Str) on vascular reactivity in young Wistar rat offspring. Vascular function was assessed in isolated aortic rings with and without endothelium by constructing concentration–effect curves to norepinephrine, acetylcholine, and sodium nitroprusside, in the presence or absence of specific pharmacological inhibitors. The contribution of α1D- and α1B-adrenergic receptors, as well as calcium-dependent mechanisms, to these responses was also examined. In parallel, systolic blood pressure, morphological characteristics of the heart and adrenal glands, and plasma corticosterone levels were determined. The results demonstrate that Str alters vascular responsiveness to norepinephrine and acetylcholine, with these effects being dependent on endothelial integrity. Moreover, Str was associated with increased systolic blood pressure, altered plasma corticosterone levels, and increased adrenal gland weight, without detectable morphological changes in the heart. Collectively, these findings indicate that prenatal stress exposure during the final week of gestation induces early functional vascular alterations associated with activation of the hypothalamic–pituitary–adrenal axis and the initial development of a hypertensive phenotype in young rats.