دورية أكاديمية
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High salt intake activates the hypothalamic-pituitary-adrenal axis, amplifies the stress response, and alters tissue glucocorticoid exposure in mice.

التفاصيل البيبلوغرافية
العنوان: High salt intake activates the hypothalamic-pituitary-adrenal axis, amplifies the stress response, and alters tissue glucocorticoid exposure in mice.
المؤلفون: Costello HM; Edinburgh Kidney, British Heart Foundation Centre for Cardiovascular Science, The Universtiy of Edinburgh, Edinburgh, EH16 4TJ, United Kingdom., Krilis G; Edinburgh Kidney, British Heart Foundation Centre for Cardiovascular Science, The Universtiy of Edinburgh, Edinburgh, EH16 4TJ, United Kingdom., Grenier C; Edinburgh Kidney, British Heart Foundation Centre for Cardiovascular Science, The Universtiy of Edinburgh, Edinburgh, EH16 4TJ, United Kingdom., Severs D; Department of Internal Medicine, Division of Nephrology and Transplantation, Erasmus Medical Center, University Medical Center Rotterdam, 3000 CA Rotterdam, The Netherlands., Czopek A; Edinburgh Kidney, British Heart Foundation Centre for Cardiovascular Science, The Universtiy of Edinburgh, Edinburgh, EH16 4TJ, United Kingdom., Ivy JR; Edinburgh Kidney, British Heart Foundation Centre for Cardiovascular Science, The Universtiy of Edinburgh, Edinburgh, EH16 4TJ, United Kingdom., Nixon M; Edinburgh Kidney, British Heart Foundation Centre for Cardiovascular Science, The Universtiy of Edinburgh, Edinburgh, EH16 4TJ, United Kingdom., Holmes MC; Edinburgh Kidney, British Heart Foundation Centre for Cardiovascular Science, The Universtiy of Edinburgh, Edinburgh, EH16 4TJ, United Kingdom., Livingstone DEW; Edinburgh Kidney, British Heart Foundation Centre for Cardiovascular Science, The Universtiy of Edinburgh, Edinburgh, EH16 4TJ, United Kingdom., Hoorn EJ; Department of Internal Medicine, Division of Nephrology and Transplantation, Erasmus Medical Center, University Medical Center Rotterdam, 3000 CA Rotterdam, The Netherlands., Dhaun N; Edinburgh Kidney, British Heart Foundation Centre for Cardiovascular Science, The Universtiy of Edinburgh, Edinburgh, EH16 4TJ, United Kingdom., Bailey MA; Edinburgh Kidney, British Heart Foundation Centre for Cardiovascular Science, The Universtiy of Edinburgh, Edinburgh, EH16 4TJ, United Kingdom.
المصدر: Cardiovascular research [Cardiovasc Res] 2023 Jul 06; Vol. 119 (8), pp. 1740-1750.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Oxford Journals Country of Publication: England NLM ID: 0077427 Publication Model: Print Cited Medium: Internet ISSN: 1755-3245 (Electronic) Linking ISSN: 00086363 NLM ISO Abbreviation: Cardiovasc Res Subsets: MEDLINE
أسماء مطبوعة: Publication: 2008- : Oxford : Oxford Journals
Original Publication: London, British Medical Assn.
مواضيع طبية MeSH: Glucocorticoids*/metabolism , Hypothalamo-Hypophyseal System*/metabolism, Humans ; Mice ; Animals ; Male ; Sodium Chloride, Dietary ; Pituitary-Adrenal System/metabolism ; Mice, Inbred C57BL ; Vasopressins/genetics ; Vasopressins/metabolism ; RNA, Messenger/genetics ; RNA, Messenger/metabolism
مستخلص: Aims: High salt intake is common and contributes to poor cardiovascular health. Urinary sodium excretion correlates directly with glucocorticoid excretion in humans and experimental animals. We hypothesized that high salt intake activates the hypothalamic-pituitary-adrenal axis activation and leads to sustained glucocorticoid excess.
Methods and Results: In male C57BL/6 mice, high salt intake for 2-8 weeks caused an increase in diurnal peak levels of plasma corticosterone. After 2 weeks, high salt increased Crh and Pomc mRNA abundance in the hypothalamus and anterior pituitary, consistent with basal hypothalamic-pituitary-adrenal axis activation. Additionally, high salt intake amplified glucocorticoid response to restraint stress, indicative of enhanced axis sensitivity. The binding capacity of Corticosteroid-Binding Globulin was reduced and its encoding mRNA downregulated in the liver. In the hippocampus and anterior pituitary, Fkbp5 mRNA levels were increased, indicating increased glucocorticoid exposure. The mRNA expression of the glucocorticoid-regenerating enzyme, 11β-hydroxysteroid dehydrogenase Type 1, was increased in these brain areas and in the liver. Sustained high salt intake activated a water conservation response by the kidney, increasing plasma levels of the vasopressin surrogate, copeptin. Increased mRNA abundance of Tonebp and Avpr1b in the anterior pituitary suggested that vasopressin signalling contributes to hypothalamic-pituitary-adrenal axis activation by high salt diet.
Conclusion: Chronic high salt intake amplifies basal and stress-induced glucocorticoid levels and resets glucocorticoid biology centrally, peripherally and within cells.
Competing Interests: Conflict of interest: N.D. has acted as a consultant for Retrophin. M.B. has consulted for River 2 Renal Corp.
(© The Author(s) 2022. Published by Oxford University Press on behalf of the European Society of Cardiology.)
التعليقات: Comment in: Cardiovasc Res. 2023 Jul 6;119(8):1619-1621. (PMID: 37212451)
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معلومات مُعتمدة: RE/18/5/34216 United Kingdom BHF_ British Heart Foundation; PG/16/98/32568 United Kingdom BHF_ British Heart Foundation; FS/18/20/33449 United Kingdom BHF_ British Heart Foundation; FS/16/54/32730 United Kingdom BHF_ British Heart Foundation
فهرسة مساهمة: Keywords: Cortisol; Glucocorticoid excess; Glucocorticoid receptor; Salt; Stress
المشرفين على المادة: 0 (Glucocorticoids)
0 (Sodium Chloride, Dietary)
11000-17-2 (Vasopressins)
0 (RNA, Messenger)
تواريخ الأحداث: Date Created: 20221111 Date Completed: 20230710 Latest Revision: 20231124
رمز التحديث: 20231124
مُعرف محوري في PubMed: PMC10325699
DOI: 10.1093/cvr/cvac160
PMID: 36368681
قاعدة البيانات: MEDLINE
الوصف
تدمد:1755-3245
DOI:10.1093/cvr/cvac160