دورية أكاديمية
High salt intake activates the hypothalamic-pituitary-adrenal axis, amplifies the stress response, and alters tissue glucocorticoid exposure in mice.
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) |
References: | JCI Insight. 2020 Mar 26;5(6):. (PMID: 32107343) Cell Metab. 2013 Jan 8;17(1):125-31. (PMID: 23312287) Steroids. 1998 Jul-Aug;63(7-8):401-5. (PMID: 9654646) Hypertension. 1998 Feb;31(2):569-74. (PMID: 9461223) J Clin Invest. 2017 May 1;127(5):1944-1959. (PMID: 28414295) Mol Cell Endocrinol. 2017 Feb 5;441:22-30. (PMID: 27521960) Clin Endocrinol (Oxf). 2020 Nov;93(5):539-545. (PMID: 32511774) Pharmacol Ther. 2016 Oct;166:128-35. (PMID: 27411675) J Am Assoc Lab Anim Sci. 2008 May;47(3):8-15. (PMID: 18459706) Neurosci Biobehav Rev. 2022 Apr;135:104385. (PMID: 34634356) Hypertension. 2016 May;67(5):1029-37. (PMID: 26953322) Endocrinology. 2019 Jan 1;160(1):38-54. (PMID: 30364965) Hypertension. 2009 Oct;54(4):890-6. (PMID: 19635986) Eur J Cancer. 2015 Dec;51(18):2820-32. (PMID: 26589974) J Clin Invest. 2004 Jan;113(2):302-9. (PMID: 14722621) Physiol Genomics. 2010 Feb 4;40(3):158-66. (PMID: 19920212) Physiol Rev. 2013 Jul;93(3):1139-206. (PMID: 23899562) Endocrine. 2013 Feb;43(1):51-8. (PMID: 22836869) Br J Nutr. 2019 Jan;121(2):164-171. (PMID: 30375311) J Mol Endocrinol. 2003 Apr;30(2):99-108. (PMID: 12683934) Nature. 2019 Oct;574(7780):686-690. (PMID: 31645758) J Clin Endocrinol Metab. 2007 Apr;92(4):1340-6. (PMID: 17264181) Front Aging Neurosci. 2019 Mar 01;11:43. (PMID: 30881301) Neuro Endocrinol Lett. 2008 Jun;29(3):341-6. (PMID: 18580851) Hypertension. 2001 Feb;37(2 Pt 2):429-32. (PMID: 11230313) Nat Rev Nephrol. 2022 May;18(5):321-335. (PMID: 35058650) Mol Cell Biol. 2006 Oct;26(19):7236-45. (PMID: 16980625) J Clin Endocrinol Metab. 2003 Jan;88(1):277-84. (PMID: 12519866) Cell Metab. 2007 Apr;5(4):313-20. (PMID: 17403375) Curr Hypertens Rep. 2017 Nov 14;19(12):100. (PMID: 29138984) Cardiovasc Res. 2021 Apr 23;117(5):1372-1381. (PMID: 33053160) Nat Med. 2011 May;17(5):573-80. (PMID: 21499270) BMJ Open. 2013 Dec 23;3(12):e003733. (PMID: 24366578) Nat Rev Endocrinol. 2012 Dec;8(12):717-27. (PMID: 22890008) Nat Rev Endocrinol. 2016 Mar;12(3):168-76. (PMID: 26794439) J Clin Invest. 2017 May 1;127(5):1932-1943. (PMID: 28414302) Hypertension. 2011 Mar;57(3):515-520. (PMID: 21282561) Curr Opin Pharmacol. 2015 Apr;21:105-14. (PMID: 25666420) Compr Physiol. 2016 Mar 15;6(2):737-71. (PMID: 27065167) Clin Endocrinol (Oxf). 2014 May;80(5):677-84. (PMID: 23594269) J Endocrinol Invest. 1986 Jun;9(3):257-9. (PMID: 3020116) Proc Natl Acad Sci U S A. 2018 Mar 20;115(12):3138-3143. (PMID: 29507217) Proc Natl Acad Sci U S A. 2004 May 4;101(18):7088-93. (PMID: 15118095) J Clin Invest. 2003 Jul;112(1):83-90. (PMID: 12840062) Lancet. 1997 Dec 13;350(9093):1734-7. (PMID: 9413464) Behav Res Methods. 2007 May;39(2):175-91. (PMID: 17695343) J Clin Endocrinol Metab. 1966 Oct;26(10):1160-9. (PMID: 5923698) J Neurosci. 2010 May 19;30(20):6916-20. (PMID: 20484633) N Engl J Med. 2021 Sep 16;385(12):1067-1077. (PMID: 34459569) Crit Rev Biochem Mol Biol. 2005 May-Jun;40(3):129-54. (PMID: 15917397) J Clin Endocrinol Metab. 2013 Aug;98(8):3315-22. (PMID: 23783094) J Neuroendocrinol. 1998 May;10(5):363-9. (PMID: 9663650) Front Endocrinol (Lausanne). 2019 Jun 26;10:422. (PMID: 31297096) Am J Physiol Renal Physiol. 2012 Jan 15;302(2):F264-75. (PMID: 21993890) Clin Chim Acta. 1983 Jul 31;132(1):101-10. (PMID: 6193907) J Clin Endocrinol Metab. 2003 Sep;88(9):4180-5. (PMID: 12970284) Am J Physiol Renal Physiol. 2006 Jan;290(1):F177-87. (PMID: 15985652) Hypertension. 2021 Jan;77(1):158-168. (PMID: 33190558) Front Endocrinol (Lausanne). 2021 Mar 16;12:627343. (PMID: 33796071) Handb Clin Neurol. 2020;175:55-64. (PMID: 33008543) Endocrinology. 1998 Jul;139(7):3220-6. (PMID: 9645696) Circulation. 2012 Dec 11;126(24):2880-9. (PMID: 23124030) Joint Bone Spine. 2018 Jul;85(4):411-416. (PMID: 28652101) |
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 |
تدمد: | 1755-3245 |
---|---|
DOI: | 10.1093/cvr/cvac160 |