Cardiovascular effects of prenatal stress—Are there implications for cerebrovascular, cognitive and mental health outcome?

• Published in: Neuroscience and biobehavioral reviews 2020-10, Vol.117, p.78-97
• Main Authors: Müller, Julia J., Antonow-Schlorke, Iwa, Kroegel, Nasim, Rupprecht, Sven, Rakers, Florian, Witte, Otto W., Schwab, Matthias
• Format: Article
• Language: English
• Subjects: Anxiety; Autonomic nervous system; Blood pressure; Cerebral blood flow; Depression; Hypothalamus-pituitary-adrenocortical axis; Maternal-fetal circulation; Sympathetic activity; Uterine and umbilical blood flow; Vascular reactivity
• ISSN: 0149-7634; 1873-7528
• DOI: 10.1016/j.neubiorev.2018.05.024

•Maternal stress but not synthetic GC exposure affects maternal-fetal circulation.•Fetal GCs program blood pressure regulation and vascular tone in animal studies.•Increase in peripheral resistance is predominantly programmed by endothelin-1.•Increase in coronary resistance is programmed by reduced NO-mediated vasodilatation.•Gestational age and sex are important moderators in cardiovascular programming. Prenatal stress programs offspring cognitive and mental health outcome. We reviewed whether prenatal stress also programs cardiovascular dysfunction which potentially modulates cerebrovascular, cognitive and mental health disorders. We focused on maternal stress and prenatal glucocorticoid (GC) exposure which have different programming effects. While maternal stress induced cortisol is mostly inactivated by the placenta, synthetic GCs freely cross the placenta and have different receptor-binding characteristics. Maternal stress, particularly anxiety, but not GC exposure, has adverse effects on maternal-fetal circulation throughout pregnancy, probably by co-activation of the maternal sympathetic nervous system, and by raising fetal catecholamines. Both effects may impair neurodevelopment. Experimental data also suggest that severe maternal stress and GC exposure during early and mid-gestation may increase the risk for cardiovascular disorders. Human data are scarce and especially lacking for older age. Programming mechanisms include aberrations in cardiac and kidney development, and functional changes in the renin-angiotensin-aldosterone-system, stress axis and peripheral and coronary vasculature. Adequate experimental or human studies examining the consequences for cerebrovascular, cognitive and mental disorders are unavailable.