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Prenatal exposure to interleukin-6 results in hypertension and increased hypothalamic-pituitary-adrenal axis activity in adult rats.

Artikel i vetenskaplig tidskrift
Författare Anne-Maj Samuelsson
Iris Öhrn
Jovanna Dahlgren
Elias Eriksson
Bo Angelin
Björn Folkow
Agneta Holmäng
Publicerad i Endocrinology
Volym 145
Nummer/häfte 11
Sidor 4897-911
ISSN 0013-7227
Publiceringsår 2004
Publicerad vid Wallenberglaboratoriet
Institutionen för fysiologi och farmakologi, Avdelningen för farmakologi
Institutionen för kvinnors och barns hälsa, Avdelningen för pediatrik
Institutionen för fysiologi och farmakologi, Avdelningen för fysiologi
Sidor 4897-911
Språk en
Länkar dx.doi.org/10.1210/en.2004-0742
Ämnesord Adrenocorticotropic Hormone, blood, pharmacology, Age Factors, Animals, Blood Pressure, drug effects, Body Weight, physiology, Circadian Rhythm, physiology, Corticotropin-Releasing Hormone, genetics, pharmacology, Exploratory Behavior, physiology, Female, Gonadal Steroid Hormones, blood, Heart Rate, drug effects, Hydrocortisone, blood, Hypertension, chemically induced, physiopathology, Hypothalamo-Hypophyseal System, physiopathology, Interleukin-6, pharmacology, Male, Pituitary-Adrenal System, physiopathology, Pregnancy, Prenatal Exposure Delayed Effects, RNA, Messenger, analysis, Rats, Rats, Wistar, Receptors, Glucocorticoid, genetics, Receptors, Mineralocorticoid, genetics, Restraint, Physical, Stress, Psychological, physiopathology
Ämneskategorier Fysiologi

Sammanfattning

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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