Free Access
Issue
Med Sci (Paris)
Volume 31, Number 4, Avril 2015
Page(s) 389 - 396
Section M/S Revues
DOI https://doi.org/10.1051/medsci/20153104013
Published online 08 May 2015
  1. Calhoun DA, Zaman MA, Nishizaka MK. Resistant hypertension. Curr Hypertens Rep 2002 ; 4 : 221–228. [CrossRef] [PubMed] [Google Scholar]
  2. Savard S, Amar L, Plouin PF, Steichen O. Cardiovascular complications associated with primary aldosteronism: a controlled cross-sectional study. Hypertension 2013 ; 62 : 331–336. [CrossRef] [PubMed] [Google Scholar]
  3. Rossi GP, Sacchetto A, Pavan E, et al. Remodeling of the left ventricle in primary aldosteronism due to Conn’s adenoma. Circulation 1997 ; 95 : 1471–1478. [CrossRef] [PubMed] [Google Scholar]
  4. Freel EM, Mark PB, Weir RA, et al. Demonstration of blood pressure-independent noninfarct myocardial fibrosis in primary aldosteronism: a cardiac magnetic resonance imaging study. Circ Cardiovasc Imaging 2012 ; 5 : 740–747. [CrossRef] [PubMed] [Google Scholar]
  5. Rossi GP, Cesari M, Cuspidi C, et al. Long-term control of arterial hypertension and regression of left ventricular hypertrophy with treatment of primary aldosteronism. Hypertension 2013 ; 62 : 62–69. [CrossRef] [PubMed] [Google Scholar]
  6. Rossi GP, Bolognesi M, Rizzoni D, et al. Vascular remodeling and duration of hypertension predict outcome of adrenalectomy in primary aldosteronism patients. Hypertension 2008 ; 51 : 1366–1371. [CrossRef] [PubMed] [Google Scholar]
  7. Spat A, Hunyady L. Control of aldosterone secretion: a model for convergence in cellular signaling pathways. Physiol Rev 2004 ; 84 : 489–539. [CrossRef] [PubMed] [Google Scholar]
  8. Choi M, Scholl UI, Yue P, et al. K+ channel mutations in adrenal aldosterone-producing adenomas and hereditary hypertension. Science 2011 ; 331 : 768–772. [CrossRef] [PubMed] [Google Scholar]
  9. Azizan EA, Poulsen H, Tuluc P, et al. Somatic mutations in ATP1A1 and CACNA1D underlie a common subtype of adrenal hypertension. Nat Genet 2013 ; 45 : 1055–1060. [CrossRef] [PubMed] [Google Scholar]
  10. Scholl UI, Goh G, Stolting G, et al. Somatic and germline CACNA1D calcium channel mutations in aldosterone-producing adenomas and primary aldosteronism. Nat Genet 2013 ; 45 : 1050–1054. [Google Scholar]
  11. Beuschlein F, Boulkroun S, Osswald A, et al. Somatic mutations in ATP1A1 and ATP2B3 lead to aldosterone-producing adenomas and secondary hypertension. Nat Genet 2013 ; 45 : 440–444. [CrossRef] [PubMed] [Google Scholar]
  12. Monticone S, Hattangady NG, Nishimoto K, et al. Effect of KCNJ5 mutations on gene expression in aldosterone-producing adenomas and adrenocortical cells. J Clin Endocrinol Metab 2012 ; 97 : E1567–E1572. [CrossRef] [PubMed] [Google Scholar]
  13. Oki K, Plonczynski MW, Luis Lam M, et al. Potassium channel mutant KCNJ5 T158A expression in HAC-15 cells increases aldosterone synthesis. Endocrinology 2012 ; 153 : 1774–1782. [CrossRef] [PubMed] [Google Scholar]
  14. Boulkroun S, Beuschlein F, Rossi GP, et al. Prevalence, clinical, and molecular Correlates of KCNJ5 mutations in primary aldosteronism. Hypertension 2012 ; 59 : 592–598. [CrossRef] [PubMed] [Google Scholar]
  15. Fernandes-Rosa FL, Williams TA, Riester A, et al. Genetic spectrum and clinical correlates of somatic mutations in aldosterone-producing adenoma. Hypertension 2014 ; 64 : 354–361. [CrossRef] [PubMed] [Google Scholar]
  16. Williams TA, Monticone S, Schack VR, et al. Somatic ATP1A1, ATP2B3, and KCNJ5 mutations in aldosterone-producing adenomas. Hypertension 2014 ; 63 : 188–195. [CrossRef] [PubMed] [Google Scholar]
  17. Kitamoto T, Suematsu S, Matsuzawa Y, et al. Comparison of cardiovascular complications in patients with and without KCNJ5 gene mutations harboring aldosterone-producing adenomas. J Atheroscler Thromb 2014 ; doi : doi.org/10.5551/jat.24455. [Google Scholar]
  18. Rossi GP, Cesari M, Letizia C, et al. KCNJ5 gene somatic mutations affect cardiac remodelling but do not preclude cure of high blood pressure and regression of left ventricular hypertrophy in primary aldosteronism. J Hypertens 2014; 32 : 1514–1521; discussion 22. [CrossRef] [PubMed] [Google Scholar]
  19. Lifton RP, Dluhy RG, Powers M, et al. A chimaeric 11 beta-hydroxylase/aldosterone synthase gene causes glucocorticoid-remediable aldosteronism and human hypertension. Nature 1992 ; 355 : 262–265. [CrossRef] [PubMed] [Google Scholar]
  20. Stowasser M, Gordon RD. Primary aldosteronism: learning from the study of familial varieties. J Hypertens 2000 ; 18 : 1165–1176. [CrossRef] [PubMed] [Google Scholar]
  21. Gordon RD, Stowasser M, Tunny TJ, et al. Clinical and pathological diversity of primary aldosteronism, including a new familial variety. Clin Exp Pharmacol Physiol 1991 ; 18 : 283–286. [CrossRef] [PubMed] [Google Scholar]
  22. Stowasser M, Gordon RD. Familial hyperaldosteronism. J Steroid Biochem Mol Biol 2001 ; 78 : 215–229. [CrossRef] [PubMed] [Google Scholar]
  23. Medeau V, Assie G, Zennaro MC, et al. Aspect familial de l’hyperaldostéronisme primaire : analyse de familles compatibles avec un with hyperaldostéronisme primaire de type 2. Ann Endocrinol (Paris) 2005 ; 66 : 240–246. [CrossRef] [PubMed] [Google Scholar]
  24. Mulatero P, Tizzani D, Viola A, et al. Prevalence and characteristics of familial hyperaldosteronism: the PATOGEN study (Primary Aldosteronism in TOrino-GENetic forms). Hypertension 2011 ; 58 : 797–803. [CrossRef] [PubMed] [Google Scholar]
  25. Lafferty AR, Torpy DJ, Stowasser M, et al. A novel genetic locus for low renin hypertension: familial hyperaldosteronism type II maps to chromosome 7 (7p22). J Med Genet 2000 ; 37 : 831–835. [CrossRef] [PubMed] [Google Scholar]
  26. Mulatero P, Tauber P, Zennaro MC, et al. KCNJ5 mutations in European families with nonglucocorticoid remediable familial hyperaldosteronism. Hypertension 2012 ; 59 : 235–240. [CrossRef] [PubMed] [Google Scholar]
  27. Geller DS, Zhang J, Wisgerhof MV, et al. A novel form of human mendelian hypertension featuring nonglucocorticoid-remediable aldosteronism. J Clin Endocrinol Metab 2008 ; 93 : 3117–3123. [CrossRef] [PubMed] [Google Scholar]
  28. Charmandari E, Sertedaki A, Kino T, et al. A novel point mutation in the KCNJ5 gene causing primary hyperaldosteronism and early-onset autosomal dominant hypertension. J Clin Endocrinol Metab 2012 ; 97 : E1532–E1539. [CrossRef] [PubMed] [Google Scholar]
  29. Monticone S, Hattangady NG, Penton D, et al. A novel Y152C KCNJ5 mutation responsible for familial hyperaldosteronism type III. J Clin Endocrinol Metab 2013 ; 98 : E1861–E1865. [CrossRef] [PubMed] [Google Scholar]
  30. Scholl UI, Nelson-Williams C, Yue P, et al. Hypertension with or without adrenal hyperplasia due to different inherited mutations in the potassium channel KCNJ5. Proc Natl Acad Sci USA 2012 ; 109 : 2533–2538. [CrossRef] [Google Scholar]
  31. Adachi M, Muroya K, Asakura Y, et al. Discordant genotype-phenotype correlation in familial hyperaldosteronism type III with KCNJ5 gene mutation: A patient report and review of the literature. Horm Res Paediatr 2014 ; 82 : 138–142. [CrossRef] [PubMed] [Google Scholar]
  32. Murthy M, Xu S, Massimo G, et al. Role for germline mutations and a rare coding single nucleotide polymorphism within the KCNJ5 potassium channel in a large cohort of sporadic cases of primary aldosteronism. Hypertension 2014 ; 63 : 783–789. [CrossRef] [PubMed] [Google Scholar]
  33. Seccia TM, Mantero F, Letizia C, et al. Somatic mutations in the KCNJ5 gene raise the lateralization index: implications for the diagnosis of primary aldosteronism by adrenal vein sampling. J Clin Endocrinol Metab 2012 ; 97 : E2307–E2313. [CrossRef] [PubMed] [Google Scholar]
  34. Osswald A, Fischer E, Degenhart C, et al. Lack of influence of somatic mutations on steroid gradients during adrenal vein sampling in aldosterone-producing adenoma patients. Eur J Endocrinol 2013 ; 169 : 657–663. [CrossRef] [PubMed] [Google Scholar]
  35. Tauber P, Penton D, Stindl J, et al. Pharmacology and pathophysiology of mutated KCNJ5 found in adrenal aldosterone-producing adenomas. Endocrinology 2014 ; 155 : 1353–1362. [CrossRef] [PubMed] [Google Scholar]
  36. Jin W, Klem AM, Lewis JH, Lu Z. Mechanisms of inward-rectifier K+ channel inhibition by tertiapin-Q. Biochemistry 1999 ; 38 : 14294–14301. [CrossRef] [PubMed] [Google Scholar]
  37. Aritomi S, Konda T, Yoshimura M. L/N-type calcium channel blocker suppresses reflex aldosterone production induced by antihypertensive action. Heart Vessels 2012 ; 27 : 419–423. [CrossRef] [PubMed] [Google Scholar]
  38. Tanaka T, Tsutamoto T, Sakai H, et al. Comparison of the effects of efonidipine and amlodipine on aldosterone in patients with hypertension. Hypertens Res 2007 ; 30 : 691–697. [CrossRef] [PubMed] [Google Scholar]

Current usage metrics show cumulative count of Article Views (full-text article views including HTML views, PDF and ePub downloads, according to the available data) and Abstracts Views on Vision4Press platform.

Data correspond to usage on the plateform after 2015. The current usage metrics is available 48-96 hours after online publication and is updated daily on week days.

Initial download of the metrics may take a while.