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Cardiovascular Institute and Wallenberg Laboratory (A.-M.S., I.O., A.H.), 413 45 Göteborg; Göteborg Pediatric Growth Research Center and Institute for the Health of Women and Children (J.D.), 416 85 Göteborg; Institute for Physiology and Pharmacology (E.E., B.F.) and Departments of Pharmacology (E.E.) and Physiology (B.F.), University of Göteborg, 405 30 Göteborg; and Center for Metabolism and Endocrinology, Department of Medicine, and Center for Nutrition and Toxicology (B.A.), Karolinska University Hospital Huddinge, 141 86 Stockholm, Sweden
Address all correspondence and requests for reprints to: Anne-Maj Samuelsson, The Wallenberg Laboratory, Göteborg University, S-413 45 Göteborg, Sweden. E-mail: anne-maj.samuelsson{at}wlab.gu.se.
During pregnancy, systemic inflammatory responses induce cytokines that may stress the fetus and contribute to cardiovascular and neuroendocrine dysfunction in adulthood. We evaluated the effects of early and late prenatal exposure to IL-6 on mean systolic arterial pressure (MSAP) and hypothalamic-pituitary-adrenal (HPA) axis regulation in male and female rats at 5–24 wk of age. MSAP and ACTH and corticosterone levels were measured basally and in response to a novel environment, immobilization stress, and stimulation with corticotropin-releasing factor (CRF) and ACTH. In addition, mRNA expression and protein levels of glucocorticoid receptor, mineralocorticoid receptor, CRF receptor type 1, and CRF were estimated in brain areas thought to mediate central effects of corticosteroids on the HPA axis and on central neuroendocrine regulation of MSAP. Both early and late prenatal IL-6 exposure led to hypertension, which was evident in females at 5 wk of age. In adult rats, basal ACTH and corticosterone levels were elevated, the responses to stress and stimulation tests were of extended duration, and circadian rhythm during the light period was flattened and reversed. Mineralocorticoid receptor and glucocorticoid receptor mRNA expression was reduced in the hippocampus, the CRF level was increased in the hypothalamus, and CRF receptor type 1 mRNA expression was increased in the pituitary. These findings suggest that fetal stress induced by prenatal exposure to IL-6 leads to hypertension and dysregulation of HPA axis activity during adulthood.
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