Role of intrarenal angiotensin II in glucocorticoid-induced renal vasodilation

E. Kubota, Koichi Hayashi, H. Matsuda, M. Honda, H. Tokuyama, K. Okubo, M. Naitoh, K. Arakawa, T. Saruta

Research output: Contribution to journalArticlepeer-review

9 Citations (Scopus)


Background. Although glucocorticoids elicit systemic hypertension, they are also demonstrated to cause marked increases in renal blood flow. The mechanism of this alteration, however, remains undetermined. Methods. Dogs were treated with dexamethasone (DEX) for 7 days, and renal, as well as systemic hemodynamic, responses to DEX were assessed. In addition, the role of intrarenal angiotensin (ANG) II in mediating the glucocorticoid-induced renal vasodilation was examined in conscious unrestrained dogs. Results. Seven-day treatment with DEX caused prominent increases in mean arterial pressure (MAP; from 80 ± 2 to 98 ± 5 mmHg) and in renal plasma flow (RPF; from 142 ± 4 to 191 ± 7ml/min), with decreases in renal vascular resistance [RVR; from 0.26 ± 0.01 to 0.22 ± 0.01 mmHg/(ml/min)] and in the filtration fraction (FF; from 0.24 ± 0.01 to 0.20 ± 0.01). DEX treatment did not alter plasma ANG II levels, but enhanced candesartan-induced reduction in MAP. In contrast, the candesartan-induced increase in RPF (19 ± 2% increase) was completely abolished by DEX. DEX treatment markedly reduced renal tissue ANG II content (from 1.09 ± 0.07 to 0.71 ± 0.04pg/mg tissue), which paralleled the response of renal tissue angiotensin-converting enzyme (ACE) activity (-20 ± 4%). Finally, intravenous ANG II administration caused a greater reduction in RPF during the DEX treatment period (-17 ± 2% vs -11 ± 1% in the control period). Conclusions. Glucocorticoids cause hypertension, but they also cause a paradoxical decrease in RVR and increase in RPF. The renal responses to candesartan and exogenous ANG II during DEX treatment suggest that the attenuation of intrarenal ANG-mediated vascular tone plays an important role in the altered renal hemodynamics. The decreased ANG tone is likely caused by reduced ANG II formation, resulting in part from suppressed ACE activity, but not from decreased sensitivity to ANG II.

Original languageEnglish
Pages (from-to)186-192
Number of pages7
JournalClinical and experimental nephrology
Issue number3
Publication statusPublished - 2001 Nov 14


  • Angiotensin II
  • Angiotensin-converting enzyme
  • Conscious dogs
  • Glucocorticoids
  • Renal hemodynamics

ASJC Scopus subject areas

  • Physiology
  • Nephrology
  • Physiology (medical)


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