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Submitted on June 10, 2004
Accepted on July 22, 2004
NG
Cardiovascular Institute and Wallenberg Laboratory (A.-M.S., I.O., A.H.), Göteborg Pediatric Growth Research Center and Institute for the Health of Women and Children (J.D.), Institute for Physiology and Pharmacology (E.E., B.F.) and Departments of Pharmacology (E.E.) and Physiology (B.F.), University of Göteborg, Göteborg; and Center for Metabolism and Endocrinology, Department of Medicine, and Center for Nutrition and Toxicology (B.A.), Karolinska University Hospital Huddinge, Stockholm, Sweden
* To whom correspondence should be addressed. 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 weeks 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 (GR), mineralocorticoid receptor (MR), CRF receptor type 1 (CRF1), 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 weeks 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. MR and GR mRNA expression was reduced in the hippocampus, the CRF level was increased in the hypothalamus and CRF 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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