The effects of Ins2(Akita) diabetes and chronic angiotensin II infusion on cystometric properties in mice

Paul C. Dolber, Huixia Jin, Rashid Nassar, Thomas M. Coffman, Susan Gurley, Matthew O. Fraser

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

Aims Diabetes is associated with both dysfunction of the lower urinary tract (LUT) and overactivity of the renin-angiotensin system (RAS). Although it is well known that the RAS affects normal LUT function, very little is known about RAS effects on the diabetic LUT. Accordingly, we investigated the effects of chronic angiotensin II (AngII) treatment on the LUT in a model of type 1 diabetes.

Methods Ins2(Akita) diabetic mice (20 weeks old) and their age-matched background controls underwent conscious cystometric evaluation after 4 weeks of chronic AngII treatment (700 ng/kg/min by osmotic pump) or vehicle (saline).

Results Diabetic mice had compensated LUT function with bladder hypertrophy. Specifically, micturition volume, residual volume, and bladder capacity were all increased, while voiding efficiency and pressure generation were unchanged as bladder mass, contraction duration, and phasic urethral function were increased. AngII significantly increased voiding efficiency and peak voiding pressure and decreased phasic frequency irrespective of diabetic state and, in diabetic but not normoglycemic control mice, significantly decreased residual volume and increased contraction duration and nonphasic contraction duration.

Conclusions The Ins2(Akita) diabetic mice had compensated LUT function at 20 weeks of age. Even under these conditions, AngII had beneficial effects on LUT function, resulting in increased voiding efficiency. Future studies should therefore be conducted to determine whether AngII can rescue the decompensated LUT function occurring in end-stage diabetic uropathy. Neurourol. Urodynam. 34:72-78, 2015.

Original languageEnglish (US)
Pages (from-to)72-78
Number of pages7
JournalNeurourology and Urodynamics
Volume34
Issue number1
DOIs
StatePublished - Jan 1 2015
Externally publishedYes

Fingerprint

Urinary Tract
Angiotensin II
Renin-Angiotensin System
Urinary Bladder
Residual Volume
Pressure
Urination
Type 1 Diabetes Mellitus
Hypertrophy

Keywords

  • bladder
  • cystometry
  • detrusor
  • diabetic cystopathy
  • diabetic uropathy
  • lower urinary tract
  • renin-angiotensin system
  • voiding efficiency

ASJC Scopus subject areas

  • Clinical Neurology
  • Urology

Cite this

The effects of Ins2(Akita) diabetes and chronic angiotensin II infusion on cystometric properties in mice. / Dolber, Paul C.; Jin, Huixia; Nassar, Rashid; Coffman, Thomas M.; Gurley, Susan; Fraser, Matthew O.

In: Neurourology and Urodynamics, Vol. 34, No. 1, 01.01.2015, p. 72-78.

Research output: Contribution to journalArticle

Dolber, Paul C. ; Jin, Huixia ; Nassar, Rashid ; Coffman, Thomas M. ; Gurley, Susan ; Fraser, Matthew O. / The effects of Ins2(Akita) diabetes and chronic angiotensin II infusion on cystometric properties in mice. In: Neurourology and Urodynamics. 2015 ; Vol. 34, No. 1. pp. 72-78.
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AB - Aims Diabetes is associated with both dysfunction of the lower urinary tract (LUT) and overactivity of the renin-angiotensin system (RAS). Although it is well known that the RAS affects normal LUT function, very little is known about RAS effects on the diabetic LUT. Accordingly, we investigated the effects of chronic angiotensin II (AngII) treatment on the LUT in a model of type 1 diabetes.Methods Ins2(Akita) diabetic mice (20 weeks old) and their age-matched background controls underwent conscious cystometric evaluation after 4 weeks of chronic AngII treatment (700 ng/kg/min by osmotic pump) or vehicle (saline).Results Diabetic mice had compensated LUT function with bladder hypertrophy. Specifically, micturition volume, residual volume, and bladder capacity were all increased, while voiding efficiency and pressure generation were unchanged as bladder mass, contraction duration, and phasic urethral function were increased. AngII significantly increased voiding efficiency and peak voiding pressure and decreased phasic frequency irrespective of diabetic state and, in diabetic but not normoglycemic control mice, significantly decreased residual volume and increased contraction duration and nonphasic contraction duration.Conclusions The Ins2(Akita) diabetic mice had compensated LUT function at 20 weeks of age. Even under these conditions, AngII had beneficial effects on LUT function, resulting in increased voiding efficiency. Future studies should therefore be conducted to determine whether AngII can rescue the decompensated LUT function occurring in end-stage diabetic uropathy. Neurourol. Urodynam. 34:72-78, 2015.

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