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Tytuł pozycji:

Aldosterone is Aberrantly Regulated by Various Stimuli in a High Proportion of Patients with Primary Aldosteronism.

Tytuł:
Aldosterone is Aberrantly Regulated by Various Stimuli in a High Proportion of Patients with Primary Aldosteronism.
Autorzy:
St-Jean M; Division of Endocrinology, Department of Medicine and Research Center, Centre hospitalier de l'Université de Montréal (CHUM), Montréal, Québec, Canada.
Bourdeau I; Division of Endocrinology, Department of Medicine and Research Center, Centre hospitalier de l'Université de Montréal (CHUM), Montréal, Québec, Canada.
Martin M; Department of biochemistry, Clinical Department of Laboratory Medecine, Centre hospitalier de l'Université de Montréal (CHUM), Montréal, Québec, Canada.
Lacroix A; Division of Endocrinology, Department of Medicine and Research Center, Centre hospitalier de l'Université de Montréal (CHUM), Montréal, Québec, Canada.
Źródło:
The Journal of clinical endocrinology and metabolism [J Clin Endocrinol Metab] 2021 Jan 01; Vol. 106 (1), pp. e45-e60.
Typ publikacji:
Journal Article; Research Support, Non-U.S. Gov't
Język:
English
Imprint Name(s):
Publication: 2017- : New York : Oxford University Press
Original Publication: Springfield, Ill. : Charles C. Thomas
MeSH Terms:
Aldosterone/*metabolism
Hyperaldosteronism/*epidemiology
Hyperaldosteronism/*metabolism
Adrenal Cortex Neoplasms/epidemiology ; Adrenal Cortex Neoplasms/metabolism ; Adrenal Glands/metabolism ; Adrenal Glands/pathology ; Adrenocortical Adenoma/epidemiology ; Adrenocortical Adenoma/metabolism ; Adult ; Aged ; Aldosterone/blood ; Diagnostic Techniques, Endocrine ; Female ; Gonadotropin-Releasing Hormone ; Humans ; Hydrocortisone/blood ; Hyperaldosteronism/blood ; Hyperaldosteronism/diagnosis ; Hyperplasia/metabolism ; Hyperplasia/pathology ; Male ; Metabolic Networks and Pathways/physiology ; Middle Aged ; Physical Stimulation/methods ; Prevalence ; Prospective Studies ; Quebec/epidemiology ; Renin/blood
References:
J Clin Endocrinol Metab. 2008 Apr;93(4):1366-71. (PMID: 18198224)
Nat Genet. 2013 Sep;45(9):1055-60. (PMID: 23913004)
Eur J Endocrinol. 2009 Mar;160(3):443-51. (PMID: 19131502)
J Clin Endocrinol Metab. 1996 Aug;81(8):3103-11. (PMID: 8768882)
J Clin Endocrinol Metab. 2011 Sep;96(9):2771-8. (PMID: 21752891)
J Clin Endocrinol Metab. 2018 Aug 1;103(8):2926-2935. (PMID: 29726953)
Compr Physiol. 2015 Jul 1;5(3):1161-82. (PMID: 26140713)
Eur J Endocrinol. 2005 Dec;153(6):939-47. (PMID: 16322401)
Horm Metab Res. 2014 May;46(5):318-21. (PMID: 24297486)
N Engl J Med. 2013 Nov 28;369(22):2115-25. (PMID: 24283225)
Front Endocrinol (Lausanne). 2016 Jun 27;7:72. (PMID: 27445975)
J Clin Endocrinol Metab. 2006 Mar;91(3):1136-42. (PMID: 16332935)
J Am Coll Cardiol. 1983 Dec;2(6):1080-3. (PMID: 6355240)
Hypertension. 2010 Nov;56(5):885-92. (PMID: 20937967)
Trends Endocrinol Metab. 2008 Sep;19(7):231-8. (PMID: 18691899)
Endocrinology. 1995 Mar;136(3):1285-95. (PMID: 7867583)
Lancet Diabetes Endocrinol. 2017 Sep;5(9):689-699. (PMID: 28576687)
Hypertens Res. 2010 May;33(5):467-72. (PMID: 20186151)
Science. 2011 Feb 11;331(6018):768-72. (PMID: 21311022)
J Clin Endocrinol Metab. 1997 Nov;82(11):3570-3. (PMID: 9360508)
Clin Endocrinol (Oxf). 2001 May;54(5):627-32. (PMID: 11380493)
J Clin Endocrinol Metab. 2009 Mar;94(3):750-6. (PMID: 19066304)
J Clin Endocrinol Metab. 2015 May;100(5):1837-44. (PMID: 25695882)
J Clin Endocrinol Metab. 1998 Jun;83(6):2029-35. (PMID: 9626135)
Nat Genet. 2013 Sep;45(9):1050-4. (PMID: 23913001)
J Clin Endocrinol Metab. 2002 Dec;87(12):5706-13. (PMID: 12466375)
Biochem Pharmacol. 1997 Jun 1;53(11):1711-7. (PMID: 9264324)
Mol Cell Endocrinol. 2015 Jun 15;408:198-204. (PMID: 25433205)
J Clin Endocrinol Metab. 2006 Apr;91(4):1566-72. (PMID: 16449345)
Clin Endocrinol (Oxf). 2020 Mar;92(3):187-195. (PMID: 31867770)
J Hum Hypertens. 2014 May;28(5):298-302. (PMID: 24284382)
J Endocr Soc. 2017 Jan 12;1(1):57-71. (PMID: 29264446)
J Clin Endocrinol Metab. 2008 Sep;93(9):3266-81. (PMID: 18552288)
J Clin Endocrinol Metab. 2015 Apr;100(4):E550-60. (PMID: 25599386)
J Clin Endocrinol Metab. 2016 Apr;101(4):1826-35. (PMID: 26918291)
JCI Insight. 2017 Sep 21;2(18):. (PMID: 28931750)
J Clin Endocrinol Metab. 2018 Nov 1;103(11):4113-4124. (PMID: 30239841)
J Clin Endocrinol Metab. 2019 Dec 1;104(12):5867-5876. (PMID: 31408156)
J Clin Endocrinol Metab. 2002 Mar;87(3):1211-6. (PMID: 11889190)
Endocr Rev. 2018 Dec 1;39(6):1057-1088. (PMID: 30124805)
N Engl J Med. 2015 Oct 8;373(15):1429-36. (PMID: 26397949)
Endocr Res. 1998 Aug-Nov;24(3-4):845-9. (PMID: 9888585)
J Endocrinol. 2007 Oct;195(1):39-48. (PMID: 17911395)
J Clin Endocrinol Metab. 2010 May;95(5):2296-305. (PMID: 20200334)
J Clin Endocrinol Metab. 2018 Oct 1;103(10):3869-3876. (PMID: 30085035)
Eur J Endocrinol. 2011 Mar;164(3):405-12. (PMID: 21330483)
Can J Physiol Pharmacol. 2000 Dec;78(12):967-83. (PMID: 11149386)
Best Pract Res Clin Endocrinol Metab. 2018 Apr;32(2):165-187. (PMID: 29678284)
Endocr Rev. 2018 Dec 1;39(6):1029-1056. (PMID: 30007283)
Nat Genet. 2013 Apr;45(4):440-4, 444e1-2. (PMID: 23416519)
Medicine (Baltimore). 2016 May;95(20):e3659. (PMID: 27196470)
Mol Cell Endocrinol. 2009 Mar 5;300(1-2):43-50. (PMID: 19027826)
Hypertension. 2018 Oct;72(4):874-880. (PMID: 30354720)
Grant Information:
201209NMD Canada CIHR
Contributed Indexing:
Keywords: G-protein coupled receptor; aberrant regulation; aldosterone; cortisol cosecretion; primary aldosteronism
Substance Nomenclature:
33515-09-2 (Gonadotropin-Releasing Hormone)
4964P6T9RB (Aldosterone)
EC 3.4.23.15 (Renin)
WI4X0X7BPJ (Hydrocortisone)
Entry Date(s):
Date Created: 20201001 Date Completed: 20210902 Latest Revision: 20231110
Update Code:
20240105
PubMed Central ID:
PMC7765652
DOI:
10.1210/clinem/dgaa703
PMID:
33000146
Czasopismo naukowe
Context: In primary aldosteronism (PA), aldosterone secretion is relatively independent of the renin-angiotensin system, but can be regulated by several other stimuli.
Objective: To evaluate aldosterone response to several stimuli in a series of patients with PA secondary either to bilateral adrenal hyperplasia (BAH) or unilateral aldosterone-producing adenoma (APA).
Design and Setting: Prospective cohort study conducted in a university teaching hospital research center.
Patients: Forty-three patients with confirmed PA and subtyped by adrenal vein sampling (n = 39) were studied, including 11 with BAH, 28 with APA, and 4 with undefined etiology. We also studied 4 other patients with aldosterone and cortisol cosecretion.
Interventions: We systematically explored aberrant regulation of aldosterone using an in vivo protocol that included the following stimulation tests performed over 3 days under dexamethasone suppression: upright posture, mixed meal, adrenocorticotropin (ACTH) 1-24, gonadotropin-releasing hormone (GnRH), vasopressin, and serotonin R4 agonist.
Main Outcome Measures: Positive response was defined as >50% renin or ACTH-independent increase in plasma aldosterone/cortisol concentration following the various stimulation tests.
Results: Renin-independent aldosterone secretion increased in response to several aberrant stimuli (upright posture, GnRH) in up to 83% of patients with APA or BAH in whom ACTH 1-24 and HT4R agonists also produced aldosterone oversecretion in all patients. The mean significant aberrant responses per patient was similar in BAH (4.6) and in APA (4.0).
Conclusions: Aldosterone secretion in PA is relatively autonomous from the renin-angiotensin system, but is highly regulated by several other stimuli, which contributes to the large variability of aldosterone levels in PA patients.
(© The Author(s) 2020. Published by Oxford University Press on behalf of the Endocrine Society. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

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