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Front Physiol. 2021 May 25;12:651246. doi: 10.3389/fphys.2021.651246. eCollection 2021.

Cardiac Natriuretic Peptide Profiles in Chronic Hypertension by Single or Sequentially Combined Renovascular and DOCA-Salt Treatments.

Frontiers in physiology

Carolina S Cerrudo, Susana Cavallero, Martín Rodríguez Fermepín, Germán E González, Martín Donato, Nicolás M Kouyoumdzian, Ricardo J Gelpi, Cecilia M Hertig, Marcelo R Choi, Belisario E Fernández

Affiliations

  1. Facultad de Farmacia y Bioquímica, Cátedras de Fisiopatología y Anatomía e Histología, Universidad de Buenos Aires, Buenos Aires, Argentina.
  2. Facultad de Medicina, CONICET, Instituto de Fisiopatología Cardiovascular, Universidad de Buenos Aires, Buenos Aires, Argentina.
  3. Instituto Alberto C. Taquini de Investigaciones en Medicina Traslacional (IATIMET), Universidad de Buenos Aires, CONICET, Buenos Aires, Argentina.
  4. Instituto de Ingeniería Genética y Biología Molecular (INGEBI), CONICET, Buenos Aires, Argentina.
  5. Instituto Universitario de Ciencias de la Salud, Fundación H. A. Barceló, Buenos Aires, Argentina.

PMID: 34113261 PMCID: PMC8185994 DOI: 10.3389/fphys.2021.651246

Abstract

The involvement of natriuretic peptides was studied during the hypertrophic remodeling transition mediated by sequential exposure to chronic hemodynamic overload. We induced hypertension in rats by pressure (renovascular) or volume overload (DOCA-salt) during 6 and 12 weeks of treatment. We also studied the consecutive combination of both models in inverse sequences: RV 6 weeks/DS 6 weeks and DS 6 weeks/RV 6 weeks. All treated groups developed hypertension. Cardiac hypertrophy and left ventricular ANP gene expression were more pronounced in single DS than in single RV groups. BNP gene expression was positively correlated with left ventricular hypertrophy only in RV groups, while ANP gene expression was positively correlated with left ventricular hypertrophy only in DS groups. Combined models exhibited intermediate values between those of single groups at 6 and 12 weeks. The latter stimulus associated to the second applied overload is less effective than the former to trigger cardiac hypertrophy and to increase ANP and BNP gene expression. In addition, we suggest a correlation of ANP synthesis with volume overload and of BNP synthesis with pressure overload-induced hypertrophy after a prolonged treatment. Volume and pressure overload may be two mechanisms, among others, involved in the differential regulation of ANP and BNP gene expression in hypertrophied left ventricles. Plasma ANP levels reflect a response to plasma volume increase and volume overload, while circulating BNP levels seem to be regulated by cardiac BNP synthesis and ventricular hypertrophy.

Copyright © 2021 Cerrudo, Cavallero, Rodríguez Fermepín, González, Donato, Kouyoumdzian, Gelpi, Hertig, Choi and Fernández.

Keywords: B type natriuretic peptide; DOCA-Salt hypertension; atrial natriuretic factor; cardiac hypertrophy; natriuretic peptides system; rat models; renovascular hypertension

Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

References

  1. Circ Res. 1975 Feb;36(2):300-9 - PubMed
  2. Int J Mol Sci. 2019 Feb 13;20(4): - PubMed
  3. Nat Rev Cardiol. 2020 Nov;17(11):698-717 - PubMed
  4. Bull Exp Biol Med. 2020 Jun;169(2):197-200 - PubMed
  5. J Hypertens. 1992 Aug;10(8):725-32 - PubMed
  6. J Am Coll Cardiol. 1992 Jun;19(7):1550-8 - PubMed
  7. Hypertension. 1999 Jun;33(6):1342-7 - PubMed
  8. J Hypertens. 2007 Sep;25(9):1940-50 - PubMed
  9. Front Physiol. 2019 Apr 16;10:435 - PubMed
  10. Peptides. 2019 Jan;111:18-25 - PubMed
  11. Am J Physiol Heart Circ Physiol. 2016 Nov 1;311(5):H1287-H1296 - PubMed
  12. Hypertension. 1988 Oct;12(4):405-10 - PubMed
  13. Hypertension. 1992 Feb;19(2):206-11 - PubMed
  14. J Pharmacol Exp Ther. 2010 Jul;334(1):87-98 - PubMed
  15. Eur Heart J. 2020 Mar 1;41(9):1006-1020 - PubMed
  16. Hypertension. 2003 Mar;41(3):540-5 - PubMed
  17. Hypertension. 2019 Jun;73(6):e87-e120 - PubMed
  18. Science. 1986 Mar 7;231(4742):1145-7 - PubMed
  19. Mol Cell Biochem. 2002 Aug;237(1-2):1-10 - PubMed
  20. Am J Physiol Heart Circ Physiol. 2000 Jul;279(1):H93-H101 - PubMed
  21. Am J Hypertens. 1997 Nov;10(11):1208-15 - PubMed
  22. Curr Protoc Mouse Biol. 2011 Mar 1;1:71-83 - PubMed
  23. Am J Hypertens. 1995 Mar;8(3):301-10 - PubMed
  24. Cardiovasc Res. 2001 Mar;49(4):808-16 - PubMed
  25. Am J Physiol. 1990 Aug;259(2 Pt 2):H324-32 - PubMed
  26. Endocr Rev. 2003 Jun;24(3):341-56 - PubMed
  27. J Hypertens. 1991 Apr;9(4):289-301 - PubMed
  28. J Theor Biol. 2008 Sep 7;254(1):178-96 - PubMed
  29. PLoS One. 2015 Aug 07;10(8):e0134579 - PubMed
  30. Lancet. 2006 Jan 28;367(9507):356-67 - PubMed
  31. Am J Physiol Heart Circ Physiol. 2002 Mar;282(3):H1127-34 - PubMed
  32. Am J Physiol Heart Circ Physiol. 2010 Apr;298(4):H1290-9 - PubMed
  33. Curr Hypertens Rep. 2017 Apr;19(4):32 - PubMed
  34. Hypertension. 2000 Dec;36(6):995-1001 - PubMed
  35. Regul Pept. 2005 Jun 30;128(3):203-10 - PubMed
  36. Am J Physiol Regul Integr Comp Physiol. 2010 Dec;299(6):R1500-10 - PubMed
  37. Am J Physiol Heart Circ Physiol. 2005 Jun;288(6):H2702-7 - PubMed
  38. Biochem Biophys Res Commun. 1990 Dec 14;173(2):632-8 - PubMed
  39. Pflugers Arch. 2001 May;442(2):212-7 - PubMed
  40. Biochim Biophys Acta. 2013 Dec;1832(12):2403-13 - PubMed
  41. Cell Mol Life Sci. 2020 Dec;77(24):5121-5130 - PubMed
  42. Circ Res. 1984 Nov;55(5):580-4 - PubMed
  43. Curr Cardiol Rev. 2010 Nov;6(4):291-7 - PubMed
  44. Vascul Pharmacol. 2004 Feb;41(1):15-20 - PubMed
  45. Hypertension. 2018 Sep;72(3):549-558 - PubMed
  46. Nihon Naibunpi Gakkai Zasshi. 1995 May 20;71(4):587-96 - PubMed

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