Display options
Cite
Majid DSA, Mahaffey E, Castillo A, et al. Angiotensin II-induced renal angiotensinogen formation is enhanced in mice lacking tumor necrosis factor-alpha type 1 receptor. Physiol Rep. 2021;9(16):e14990doi: 10.14814/phy2.14990.
Majid, D. S. A., Mahaffey, E., Castillo, A., Prieto, M. C., & Navar, L. G. (2021). Angiotensin II-induced renal angiotensinogen formation is enhanced in mice lacking tumor necrosis factor-alpha type 1 receptor. Physiological reports, 9(16), e14990. https://doi.org/10.14814/phy2.14990
Majid, Dewan S A, et al. "Angiotensin II-induced renal angiotensinogen formation is enhanced in mice lacking tumor necrosis factor-alpha type 1 receptor." Physiological reports vol. 9,16 (2021): e14990. doi: https://doi.org/10.14814/phy2.14990
Majid DSA, Mahaffey E, Castillo A, Prieto MC, Navar LG. Angiotensin II-induced renal angiotensinogen formation is enhanced in mice lacking tumor necrosis factor-alpha type 1 receptor. Physiol Rep. 2021 Aug;9(16):e14990. doi: 10.14814/phy2.14990. PMID: 34427402; PMCID: PMC8383705.
Copy Download .nbib Format: NLM
Share it on

Physiol Rep. 2021 Aug;9(16):e14990. doi: 10.14814/phy2.14990.

Angiotensin II-induced renal angiotensinogen formation is enhanced in mice lacking tumor necrosis factor-alpha type 1 receptor.

Physiological reports

Dewan S A Majid, Eamonn Mahaffey, Alexander Castillo, Minolfa C Prieto, L Gabriel Navar

Affiliations

  1. Department of Physiology, Hypertension & Renal Center of Excellence, Tulane University School of Medicine, New Orleans, Louisiana, USA.

PMID: 34427402 PMCID: PMC8383705 DOI: 10.14814/phy2.14990

Abstract

In hypertension induced by angiotensin II (AngII) administration with high salt (HS) intake, intrarenal angiotensinogen (AGT) and tumor necrosis factor-alpha (TNF-α) levels increase. However, TNF-α has been shown to suppress AGT formation in cultured renal proximal tubular cells. We examined the hypothesis that elevated AngII levels during HS intake reduces TNF-α receptor type 1 (TNFR1) activity in the kidneys, thus facilitating increased intrarenal AGT formation. The responses to HS diet (4% NaCl) with chronic infusion of AngII (25 ng/min) via implanted minipump for 4 weeks were assessed in wild-type (WT) and knockout (KO) mice lacking TNFR1 or TNFR2 receptors. Blood pressure was measured by tail-cuff plethysmography, and 24-h urine samples were collected using metabolic cages prior to start (0 day) and at the end of 2nd and 4th week periods. The urinary excretion rate of AGT (uAGT; marker for intrarenal AGT) was measured using ELISA. HS +AngII treatment for 4 weeks increased mean arterial pressure (MAP) in all strains of mice. However, the increase in MAP in TNFR1KO (77 ± 2 to 115 ± 3 mmHg; n = 7) was significantly greater (p < 0.01) than in WT (76 ± 1 to 102 ± 2 mmHg; n = 7) or in TNFR2KO (78 ± 2 to 99 ± 5 mmHg; n = 6). The increase in uAGT at 4th week was also greater (p < 0.05) in TNFR1KO mice (6 ± 2 to 167 ± 75 ng/24 h) than that in WT (6 ± 3 to 46 ± 16 ng/24 h) or in TNFR2KO mice (8 ± 7 to 65 ± 44 ng/24 h). The results indicate that TNFR1 exerts a protective role by mitigating intrarenal AGT formation induced by elevated AngII and HS intake.

© 2021 The Authors. Physiological Reports published by Wiley Periodicals LLC on behalf of The Physiological Society and the American Physiological Society.

Keywords: High salt intake; TNF-α receptors; angiotensin II; angiotensinogen; renal injury

References

  1. Am J Physiol Renal Physiol. 2010 Jul;299(1):F217-24 - PubMed
  2. Can J Cardiol. 2013 May;29(5):543-8 - PubMed
  3. Clin Exp Pharmacol Physiol. 2007 Sep;34(9):946-52 - PubMed
  4. Am J Hypertens. 2014 Nov;27(11):1327-37 - PubMed
  5. Am J Physiol Renal Physiol. 2011 Jul;301(1):F94-100 - PubMed
  6. Hypertension. 2014 Dec;64(6):1275-81 - PubMed
  7. Am J Physiol Renal Physiol. 2007 Sep;293(3):F938-45 - PubMed
  8. Hypertension. 2008 May;51(5):1345-51 - PubMed
  9. Adv Exp Med Biol. 2011;691:471-80 - PubMed
  10. Am J Physiol Renal Physiol. 2012 Jan 1;302(1):F85-94 - PubMed
  11. Hypertension. 2018 Jul;72(1):19-23 - PubMed
  12. Am J Physiol Renal Physiol. 2008 Dec;295(6):F1836-44 - PubMed
  13. Am J Physiol Renal Physiol. 2017 Oct 1;313(4):F1005-F1008 - PubMed
  14. Am J Physiol Renal Physiol. 2014 Sep 1;307(5):F499-508 - PubMed
  15. Hypertens Res. 2010 Jun;33(6):515-20 - PubMed
  16. Am J Physiol Cell Physiol. 2010 Oct;299(4):C750-9 - PubMed
  17. Cell Physiol Biochem. 2018;48(1):339-347 - PubMed
  18. Hypertens Res. 2017 May;40(5):413-422 - PubMed
  19. Curr Hypertens Rev. 2015;11(1):38-48 - PubMed
  20. Am J Physiol Renal Physiol. 2006 May;290(5):F1110-7 - PubMed
  21. Am J Physiol Renal Physiol. 2010 Nov;299(5):F1141-50 - PubMed
  22. Am J Physiol Renal Physiol. 2010 Sep;299(3):F656-63 - PubMed
  23. Am J Physiol Renal Physiol. 2013 Apr 1;304(7):F991-9 - PubMed
  24. Am J Physiol Renal Physiol. 2012 Jun 15;302(12):F1650-7 - PubMed
  25. Am J Pathol. 2002 Nov;161(5):1679-93 - PubMed
  26. Hypertension. 2011 Mar;57(3):355-62 - PubMed
  27. Am J Physiol Regul Integr Comp Physiol. 2008 Jan;294(1):R76-83 - PubMed
  28. Physiol Rep. 2014 Feb 10;2(2):e00228 - PubMed
  29. Hypertension. 2011 Feb;57(2):132-40 - PubMed
  30. Kidney Int Suppl. 2002 Dec;(82):S12-22 - PubMed
  31. Hypertension. 2003 Jan;41(1):42-9 - PubMed
  32. Am J Physiol Renal Physiol. 2013 Oct 1;305(7):F1031-41 - PubMed
  33. J Exp Med. 2007 Oct 1;204(10):2449-60 - PubMed
  34. Hypertension. 2020 Dec;76(6):1744-1752 - PubMed
  35. Sci Rep. 2016 Feb 26;6:21960 - PubMed
  36. Am J Physiol Renal Physiol. 2008 Sep;295(3):F772-9 - PubMed
  37. Hypertension. 2009 Feb;53(2):344-50 - PubMed
  38. Am J Physiol Renal Physiol. 2008 Jul;295(1):F283-9 - PubMed

Publication Types

Grant support