Display options
Cite
Ikeda K, Isaka T, Fujioka K, et al. Suppression of aldosterone synthesis and secretion by ca(2+) channel antagonists. Int J Endocrinol. 2012;2012:519467doi: 10.1155/2012/519467.
Ikeda, K., Isaka, T., Fujioka, K., Manome, Y., & Tojo, K. (2012). Suppression of aldosterone synthesis and secretion by ca(2+) channel antagonists. International journal of endocrinology, 2012519467. https://doi.org/10.1155/2012/519467
Ikeda, Keiichi, et al. "Suppression of aldosterone synthesis and secretion by ca(2+) channel antagonists." International journal of endocrinology vol. 2012 (2012): 519467. doi: https://doi.org/10.1155/2012/519467
Ikeda K, Isaka T, Fujioka K, Manome Y, Tojo K. Suppression of aldosterone synthesis and secretion by ca(2+) channel antagonists. Int J Endocrinol. 2012;2012:519467. doi: 10.1155/2012/519467. Epub 2012 Oct 11. PMID: 23097668; PMCID: PMC3477571.
Copy Download .nbib Format: NLM
Share it on

Int J Endocrinol. 2012;2012:519467. doi: 10.1155/2012/519467. Epub 2012 Oct 11.

Suppression of aldosterone synthesis and secretion by ca(2+) channel antagonists.

International journal of endocrinology

Keiichi Ikeda, Tsuyoshi Isaka, Kouki Fujioka, Yoshinobu Manome, Katsuyoshi Tojo

Affiliations

  1. Department of Molecular Cell Biology, Institute of DNA Medicine, Research Center for Medical Sciences, The Jikei University School of Medicine, 3-25-8 Nishishinbashi, Minato-ku, Tokyo 105-8461, Japan.

PMID: 23097668 PMCID: PMC3477571 DOI: 10.1155/2012/519467

Abstract

Aldosterone, a specific mineralocorticoid receptor (MR) agonist and a key player in the development of hypertension, is synthesized as a final product of renin-angiotensin-aldosterone system. Hypertension can be generally treated by negating the effects of angiotensin II through the use of angiotensin-converting enzyme inhibitors (ACE-Is) or angiotensin II type 1 receptor antagonists (ARBs). However, the efficacy of angiotensin II blockade by such drugs is sometimes diminished by the so-called "aldosterone breakthrough" effect, by which ACE-Is or ARBs (renin-angiotensin system (RAS) inhibitors) gradually lose their effectiveness against hypertension due to the overproduction of aldosterone, known as primary aldosteronism. Although MR antagonists are used to antagonize the effects of aldosterone, these drugs may, however, give rise to life-threatening adverse actions, such as hyperkalemia, particularly when used in conjunction with RAS inhibitors. Recently, several groups have reported that some dihydropyridine Ca(2+) channel blockers (CCBs) have inhibitory actions on aldosterone production in in vitro and in the clinical setting. Therefore, the use of such dihydropyridine CCBs to treat aldosterone-related hypertension may prove beneficial to circumvent such therapeutic problems. In this paper, we discuss the mechanism of action of CCBs on aldosterone production and clinical perspectives for CCB use to inhibit MR activity in hypertensive patients.

References

  1. Hypertens Res. 2007 Sep;30(9):815-22 - PubMed
  2. Hypertens Res. 2009 Dec;32(12):1148-54 - PubMed
  3. N Engl J Med. 1999 Sep 2;341(10):709-17 - PubMed
  4. J Clin Invest. 1996 Jul 15;98(2):460-6 - PubMed
  5. Endocrinology. 1997 Feb;138(2):835-8 - PubMed
  6. N Engl J Med. 2011 Jan 6;364(1):11-21 - PubMed
  7. Can J Cardiol. 2011 Jul-Aug;27(4):415-433.e1-2 - PubMed
  8. Hypertens Res. 2012 Mar;35(3):287-94 - PubMed
  9. Hypertension. 2008 Mar;51(3):742-8 - PubMed
  10. Hypertens Res. 2008 Aug;31(8):1499-508 - PubMed
  11. Am J Physiol. 1999 May;276(5):F674-83 - PubMed
  12. Tohoku J Exp Med. 2011;224(4):263-71 - PubMed
  13. Hypertens Res. 2007 Jul;30(7):621-6 - PubMed
  14. J Pharmacol Exp Ther. 2009 Feb;328(2):621-7 - PubMed
  15. Eur J Pharmacol. 1999 May 28;373(1):93-100 - PubMed
  16. Eur J Pharmacol. 2010 Jun 10;635(1-3):49-55 - PubMed
  17. J Steroid Biochem Mol Biol. 2004 Oct;92(3):209-18 - PubMed
  18. Hypertens Res. 2011 Feb;34(2):193-201 - PubMed
  19. Curr Opin Nephrol Hypertens. 2012 Mar;21(2):147-56 - PubMed
  20. Hypertension. 1995 Jun;25(6):1129-34 - PubMed
  21. Eur J Biochem. 1977 Aug 15;78(1):231-8 - PubMed
  22. J Hypertens. 2010 Jun;28(6):1321-9 - PubMed
  23. N Engl J Med. 2003 Apr 3;348(14):1309-21 - PubMed
  24. J Am Soc Hypertens. 2010 Sep-Oct;4(5):215-8 - PubMed
  25. Mol Cell Endocrinol. 2001 Apr 25;175(1-2):157-71 - PubMed
  26. Endocrinology. 1996 Nov;137(11):4817-26 - PubMed
  27. Endocrinology. 1993 Mar;132(3):1035-43 - PubMed
  28. J Hypertens. 2011 Aug;29(8):1649-59 - PubMed
  29. J Hypertens. 2007 Jun;25(6):1105-87 - PubMed
  30. Endocr Rev. 2011 Feb;32(1):81-151 - PubMed
  31. Hypertens Res. 2011 Feb;34(2):268-73 - PubMed
  32. Am J Hypertens. 2003 Sep;16(9 Pt 1):781-8 - PubMed
  33. J Am Soc Hypertens. 2009 Jan-Feb;3(1):52-68 - PubMed
  34. Biochem J. 1995 Jan 15;305 ( Pt 2):569-76 - PubMed
  35. Curr Drug Saf. 2007 Jan;2(1):71-7 - PubMed
  36. J Clin Hypertens (Greenwich). 2008 Jul;10(7):534-40 - PubMed
  37. Eur J Pharmacol. 2009 Jun 24;613(1-3):100-7 - PubMed
  38. Hypertension. 2003 Dec;42(6):1206-52 - PubMed
  39. Hypertens Res. 2009 Jan;32(1):3-107 - PubMed
  40. J Pharmacol Exp Ther. 1998 Dec;287(3):824-31 - PubMed
  41. Hypertens Res. 2009 Aug;32(8):670-4 - PubMed
  42. Endocr Dev. 2008;13:1-18 - PubMed
  43. Circulation. 2003 Oct 14;108(15):1831-8 - PubMed
  44. Curr Hypertens Rep. 2006 Jun;8(3):262-8 - PubMed
  45. Heart Vessels. 2012 Jul;27(4):419-23 - PubMed
  46. Eur J Pharmacol. 2008 Apr 28;584(2-3):424-34 - PubMed
  47. Hypertens Res. 2011 Apr;34(4):423-30 - PubMed
  48. Med Arh. 2010;64(5):295-9 - PubMed
  49. Med Clin North Am. 2009 May;93(3):569-82 - PubMed
  50. Ther Adv Cardiovasc Dis. 2012 Apr;6(2):81-91 - PubMed
  51. Curr Med Res Opin. 2010 Sep;26(9):2263-76 - PubMed
  52. Eur J Pharmacol. 2009 Mar 1;605(1-3):49-52 - PubMed
  53. Eur J Pharmacol. 1998 May 22;349(2-3):351-7 - PubMed
  54. J Endocrinol. 2010 Jan;204(1):67-74 - PubMed
  55. J Cardiovasc Pharmacol. 2006 Jan;47(1):133-8 - PubMed
  56. Am J Hypertens. 2012 Jul;25(7):818-26 - PubMed

Publication Types