Role of intrarenal angiotensin II in glucocorticoid-induced renal vasodilation

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

Research output: Contribution to journalArticle

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Abstract

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
Volume5
Issue number3
DOIs
Publication statusPublished - 2001

Fingerprint

Vasodilation
Angiotensin II
Dexamethasone
Glucocorticoids
Kidney
Angiotensins
Peptidyl-Dipeptidase A
Hemodynamics
Dogs
Hypertension
Renal Plasma Flow
Renal Circulation
Vascular Resistance
Blood Vessels
Arterial Pressure
candesartan

Keywords

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

ASJC Scopus subject areas

  • Nephrology

Cite this

Role of intrarenal angiotensin II in glucocorticoid-induced renal vasodilation. / Kubota, E.; Hayashi, K.; Matsuda, H.; Honda, M.; Tokuyama, Hirobumi; Okubo, K.; Naitoh, M.; Arakawa, K.; Saruta, T.

In: Clinical and Experimental Nephrology, Vol. 5, No. 3, 2001, p. 186-192.

Research output: Contribution to journalArticle

Kubota, E, Hayashi, K, Matsuda, H, Honda, M, Tokuyama, H, Okubo, K, Naitoh, M, Arakawa, K & Saruta, T 2001, 'Role of intrarenal angiotensin II in glucocorticoid-induced renal vasodilation', Clinical and Experimental Nephrology, vol. 5, no. 3, pp. 186-192. https://doi.org/10.1007/s101570170009
Kubota, E. ; Hayashi, K. ; Matsuda, H. ; Honda, M. ; Tokuyama, Hirobumi ; Okubo, K. ; Naitoh, M. ; Arakawa, K. ; Saruta, T. / Role of intrarenal angiotensin II in glucocorticoid-induced renal vasodilation. In: Clinical and Experimental Nephrology. 2001 ; Vol. 5, No. 3. pp. 186-192.
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abstract = "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.",
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T1 - Role of intrarenal angiotensin II in glucocorticoid-induced renal vasodilation

AU - Kubota, E.

AU - Hayashi, K.

AU - Matsuda, H.

AU - Honda, M.

AU - Tokuyama, Hirobumi

AU - Okubo, K.

AU - Naitoh, M.

AU - Arakawa, K.

AU - Saruta, T.

PY - 2001

Y1 - 2001

N2 - 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.

AB - 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.

KW - Angiotensin II

KW - Angiotensin-converting enzyme

KW - Conscious dogs

KW - Glucocorticoids

KW - Renal hemodynamics

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