Effects of histamine and the h2 receptor antagonist ranitidine on ischemia-induced acute renal failure: involvement of IL-6 and vascular endothelial growth factor

Kidney Blood Press Res. 2004;27(2):105-13. doi: 10.1159/000077350. Epub 2004 Mar 17.

Abstract

Background: Vascular endothelial growth factor (VEGF) exerts cytoprotective, antiapoptotic and proangiogenic effects; its synthesis is induced by hypoxia, several cytokines and histamine. The effects of histamine and the H2 receptor antagonist ranitidine on renal VEGF and IL-6 synthesis were investigated in a well-established rat model of renal ischemia/reperfusion injury.

Methods: Following 7 days of pretreatment with histamine (H group; n = 12), ranitidine (R group; n = 10) or vehicle (controls; n = 13), the left vascular pedicle was clamped for 50 min in uninephrectomized male rats and survival assessed in the different treatment groups. Additionally, renal IL-6 mRNA expression, as well as VEGF mRNA and protein abundance were measured in the three treatment groups following pretreatment only, 2 and 16 h after 50 min of renal ischemia (n = 6/group/timepoint).

Results: Ranitidine significantly increased, while histamine significantly decreased survival following renal ischemia. Renal IL-6 mRNA expression increased 2 h after reperfusion in all groups and decreased thereafter, with the lowest level observed in the R group. While VEGF mRNA did not change in controls, histamine increased, whereas ranitidine decreased its expression during the follow-up. Two hours after ischemia a twofold increase in renal VEGF protein abundance was observed in controls and the H group and significantly higher values were noted in the R group at this time point. A further increase in VEGF protein was only present in the H group 16 h after reperfusion.

Conclusion: These results indicate an important role of histamine in kidney damage following renal ischemia. The beneficial effects of ranitidine were partly mediated by decreased IL-6 and VEGF mRNA expression and significant early increase in renal VEGF abundance.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acute Kidney Injury / blood
  • Acute Kidney Injury / etiology*
  • Acute Kidney Injury / pathology
  • Acute Kidney Injury / physiopathology
  • Animals
  • Histamine / metabolism*
  • Histamine H2 Antagonists / pharmacology*
  • Interleukin-6 / genetics
  • Ischemia / complications*
  • Kidney / pathology
  • Male
  • RNA, Messenger / metabolism
  • Ranitidine / pharmacology*
  • Rats
  • Rats, Wistar
  • Renal Circulation*
  • Reperfusion Injury / pathology
  • Survival Analysis
  • Vascular Endothelial Growth Factor A / genetics
  • Vascular Endothelial Growth Factor A / metabolism

Substances

  • Histamine H2 Antagonists
  • Interleukin-6
  • RNA, Messenger
  • Vascular Endothelial Growth Factor A
  • Histamine
  • Ranitidine