Acute Urinary Bladder Distension Triggers ICAM-1-mediated Renal Oxidative Injury via the Norepinephrine-renin-angiotensin II System in Rats

Show Shing Chen, Wang Chuan Chen, Satoshi Hayakawa, Ping Chia Li, Chiang Ting Chien

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

Background/Purpose: Acute urinary bladder distension (AUBD) can activate bladder mechanical afferent and renal sympathetic nerves, which contributes to renal vasoconstriction. We hypothesized that AUBD-induced renal sympathetic activation may contribute to inflammatory responses and end-organ damage via activation of angiotensin-II-receptor-mediated intercellular adhesion molecule-1 (ICAM-1) expression and leukocyte infiltration in the kidney. Methods: We evaluated the effect of 2 hours of AUBD induced by a threshold volume (micturition volume) on renal oxygen tension, microcirculation, renal reactive oxygen species (ROS) and monocyte/ macrophage (ED-1) infiltration, and ICAM-1 expression in the kidneys of urethane-anesthetized female Wistar rats. Bilateral ureteral dissection, renal denervation and intrarenal angiotensin II type 1 receptor blockade (2 mg/kg valsartan) were used to determine their roles in AUBD-induced renal oxidative stress. Results: Our results showed that AUBD evoked hypertension, a reduction in cortex oxygen tension and microcirculation, and increased renal ROS production, which were caused by increased perivascular and interstitial monocyte/macrophage infiltration and endothelial ICAM-1 overexpression. Renal denervation and angiotensin II type 1 receptor antagonist, but not bilateral ureter dissection, abolished the reduction in cortex oxygen tension and microcirculation, increased renal ROS production, increased perivascular monocyte/macrophage infiltration, and led to endothelial ICAM-1 overexpression in the kidney. Conclusion: Acute urinary retention enhances renal sympathetic activity, which causes renal vasoconstriction and increases oxidative stress, adhesion-molecule expression and leukocyte infiltration in the rat kidney via the angiotensin II type 1 receptor pathway.

Original languageEnglish
Pages (from-to)627-635
Number of pages9
JournalJournal of the Formosan Medical Association
Volume108
Issue number8
DOIs
Publication statusPublished - 2009 Aug 1

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Intercellular Adhesion Molecule-1
Renin-Angiotensin System
Angiotensin II
Norepinephrine
Urinary Bladder
Kidney
Wounds and Injuries
Microcirculation
Monocytes
Reactive Oxygen Species
Angiotensin Type 1 Receptor
Macrophages
Valsartan
Denervation
Oxygen
Vasoconstriction
Dissection
Oxidative Stress
Angiotensin II Type 1 Receptor Blockers
Angiotensin Receptors

Keywords

  • angiotensin II
  • intercellular adhesion molecule-1
  • kidney
  • oxidative stress
  • urinary retention

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Acute Urinary Bladder Distension Triggers ICAM-1-mediated Renal Oxidative Injury via the Norepinephrine-renin-angiotensin II System in Rats. / Chen, Show Shing; Chen, Wang Chuan; Hayakawa, Satoshi; Li, Ping Chia; Chien, Chiang Ting.

In: Journal of the Formosan Medical Association, Vol. 108, No. 8, 01.08.2009, p. 627-635.

Research output: Contribution to journalArticle

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abstract = "Background/Purpose: Acute urinary bladder distension (AUBD) can activate bladder mechanical afferent and renal sympathetic nerves, which contributes to renal vasoconstriction. We hypothesized that AUBD-induced renal sympathetic activation may contribute to inflammatory responses and end-organ damage via activation of angiotensin-II-receptor-mediated intercellular adhesion molecule-1 (ICAM-1) expression and leukocyte infiltration in the kidney. Methods: We evaluated the effect of 2 hours of AUBD induced by a threshold volume (micturition volume) on renal oxygen tension, microcirculation, renal reactive oxygen species (ROS) and monocyte/ macrophage (ED-1) infiltration, and ICAM-1 expression in the kidneys of urethane-anesthetized female Wistar rats. Bilateral ureteral dissection, renal denervation and intrarenal angiotensin II type 1 receptor blockade (2 mg/kg valsartan) were used to determine their roles in AUBD-induced renal oxidative stress. Results: Our results showed that AUBD evoked hypertension, a reduction in cortex oxygen tension and microcirculation, and increased renal ROS production, which were caused by increased perivascular and interstitial monocyte/macrophage infiltration and endothelial ICAM-1 overexpression. Renal denervation and angiotensin II type 1 receptor antagonist, but not bilateral ureter dissection, abolished the reduction in cortex oxygen tension and microcirculation, increased renal ROS production, increased perivascular monocyte/macrophage infiltration, and led to endothelial ICAM-1 overexpression in the kidney. Conclusion: Acute urinary retention enhances renal sympathetic activity, which causes renal vasoconstriction and increases oxidative stress, adhesion-molecule expression and leukocyte infiltration in the rat kidney via the angiotensin II type 1 receptor pathway.",
keywords = "angiotensin II, intercellular adhesion molecule-1, kidney, oxidative stress, urinary retention",
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N2 - Background/Purpose: Acute urinary bladder distension (AUBD) can activate bladder mechanical afferent and renal sympathetic nerves, which contributes to renal vasoconstriction. We hypothesized that AUBD-induced renal sympathetic activation may contribute to inflammatory responses and end-organ damage via activation of angiotensin-II-receptor-mediated intercellular adhesion molecule-1 (ICAM-1) expression and leukocyte infiltration in the kidney. Methods: We evaluated the effect of 2 hours of AUBD induced by a threshold volume (micturition volume) on renal oxygen tension, microcirculation, renal reactive oxygen species (ROS) and monocyte/ macrophage (ED-1) infiltration, and ICAM-1 expression in the kidneys of urethane-anesthetized female Wistar rats. Bilateral ureteral dissection, renal denervation and intrarenal angiotensin II type 1 receptor blockade (2 mg/kg valsartan) were used to determine their roles in AUBD-induced renal oxidative stress. Results: Our results showed that AUBD evoked hypertension, a reduction in cortex oxygen tension and microcirculation, and increased renal ROS production, which were caused by increased perivascular and interstitial monocyte/macrophage infiltration and endothelial ICAM-1 overexpression. Renal denervation and angiotensin II type 1 receptor antagonist, but not bilateral ureter dissection, abolished the reduction in cortex oxygen tension and microcirculation, increased renal ROS production, increased perivascular monocyte/macrophage infiltration, and led to endothelial ICAM-1 overexpression in the kidney. Conclusion: Acute urinary retention enhances renal sympathetic activity, which causes renal vasoconstriction and increases oxidative stress, adhesion-molecule expression and leukocyte infiltration in the rat kidney via the angiotensin II type 1 receptor pathway.

AB - Background/Purpose: Acute urinary bladder distension (AUBD) can activate bladder mechanical afferent and renal sympathetic nerves, which contributes to renal vasoconstriction. We hypothesized that AUBD-induced renal sympathetic activation may contribute to inflammatory responses and end-organ damage via activation of angiotensin-II-receptor-mediated intercellular adhesion molecule-1 (ICAM-1) expression and leukocyte infiltration in the kidney. Methods: We evaluated the effect of 2 hours of AUBD induced by a threshold volume (micturition volume) on renal oxygen tension, microcirculation, renal reactive oxygen species (ROS) and monocyte/ macrophage (ED-1) infiltration, and ICAM-1 expression in the kidneys of urethane-anesthetized female Wistar rats. Bilateral ureteral dissection, renal denervation and intrarenal angiotensin II type 1 receptor blockade (2 mg/kg valsartan) were used to determine their roles in AUBD-induced renal oxidative stress. Results: Our results showed that AUBD evoked hypertension, a reduction in cortex oxygen tension and microcirculation, and increased renal ROS production, which were caused by increased perivascular and interstitial monocyte/macrophage infiltration and endothelial ICAM-1 overexpression. Renal denervation and angiotensin II type 1 receptor antagonist, but not bilateral ureter dissection, abolished the reduction in cortex oxygen tension and microcirculation, increased renal ROS production, increased perivascular monocyte/macrophage infiltration, and led to endothelial ICAM-1 overexpression in the kidney. Conclusion: Acute urinary retention enhances renal sympathetic activity, which causes renal vasoconstriction and increases oxidative stress, adhesion-molecule expression and leukocyte infiltration in the rat kidney via the angiotensin II type 1 receptor pathway.

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