Urinary bladder relaxation through activation of imidazoline receptors induced by agmatine is increased in diabetic rats

Tsung Chin Tsai, Chia Ho Lin, Hsien Hui Chung, Juei Tang Cheng, I-Hung Chen, Yat-Ching Tong

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

Objectives: The effect of agmatine on bladder contractility and the diabetes-induced alteration of this action were studied in the rat. Methods: Bladder strips were isolated from 9-week-old streptozotocin (STZ)-diabetic rats and control Wistar rats. Strips were hung in an organ bath for measurement of isometric tension and pre-contracted with either 1μmol/L acetylcholine (ACh) or 50mmol/L KCl. Dose-dependent relaxation of the bladder strips was studied by cumulative administration of agmatine 1-100μmol/L into the organ bath. Effects of specific imidazoline receptor (IR) antagonists on the agmatine-induced relaxation were studied. Western blotting analysis was used to measure bladder IR, sulphonylurea receptor (SUR) and inwardly rectifying K+ channel subunit 6.2 (Kir 6.2) protein levels. Results: Agmatine reduced ACh and KCl pre-contracted bladder strip tension in a dose-dependent fashion. Relaxation was significantly increased in STZ-diabetic rats. The relaxation was inhibited by BU224, a selective I2 IR antagonist; but not by efaroxan (I1 IR antagonist) or KU14R (I3 IR antagonist). Moreover, the agmatine-induced relaxation was attenuated by glibenclamide (inhibitor of KATP channel) and H-89 (inhibitor of protein kinase A), but enhanced by 3-isobutyl-1-methylxanthine (IBMX, inhibitor of cyclic AMP phosphodiesterase). Western blotting showed increased expression of bladder IR but not SUR or Kir 6.2 in the STZ-diabetic rat. Conclusion: Agmatine causes rat bladder relaxation by activation of the I2 IR, which opens KATP channels through the cyclic AMP/protein kinase A pathway. Agmatine-induced bladder relaxation in STZ-diabetic rats is increased due to a higher expression of IR.

Original languageEnglish
Pages (from-to)117-123
Number of pages7
JournalLUTS: Lower Urinary Tract Symptoms
Volume6
Issue number2
DOIs
Publication statusPublished - 2014 Jan 1

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Imidazoline Receptors
Agmatine
Urinary Bladder
Streptozocin
Sulfonylurea Receptors
1-Methyl-3-isobutylxanthine
KATP Channels
efaroxan
Cyclic AMP-Dependent Protein Kinases
Baths
Cyclic AMP
Acetylcholine
Western Blotting
Inwardly Rectifying Potassium Channel
Adenylate Kinase
Glyburide
Phosphoric Diester Hydrolases
Wistar Rats

All Science Journal Classification (ASJC) codes

  • Neurology
  • Urology

Cite this

@article{53ed741259d6478db1b73d7c0c8bb5aa,
title = "Urinary bladder relaxation through activation of imidazoline receptors induced by agmatine is increased in diabetic rats",
abstract = "Objectives: The effect of agmatine on bladder contractility and the diabetes-induced alteration of this action were studied in the rat. Methods: Bladder strips were isolated from 9-week-old streptozotocin (STZ)-diabetic rats and control Wistar rats. Strips were hung in an organ bath for measurement of isometric tension and pre-contracted with either 1μmol/L acetylcholine (ACh) or 50mmol/L KCl. Dose-dependent relaxation of the bladder strips was studied by cumulative administration of agmatine 1-100μmol/L into the organ bath. Effects of specific imidazoline receptor (IR) antagonists on the agmatine-induced relaxation were studied. Western blotting analysis was used to measure bladder IR, sulphonylurea receptor (SUR) and inwardly rectifying K+ channel subunit 6.2 (Kir 6.2) protein levels. Results: Agmatine reduced ACh and KCl pre-contracted bladder strip tension in a dose-dependent fashion. Relaxation was significantly increased in STZ-diabetic rats. The relaxation was inhibited by BU224, a selective I2 IR antagonist; but not by efaroxan (I1 IR antagonist) or KU14R (I3 IR antagonist). Moreover, the agmatine-induced relaxation was attenuated by glibenclamide (inhibitor of KATP channel) and H-89 (inhibitor of protein kinase A), but enhanced by 3-isobutyl-1-methylxanthine (IBMX, inhibitor of cyclic AMP phosphodiesterase). Western blotting showed increased expression of bladder IR but not SUR or Kir 6.2 in the STZ-diabetic rat. Conclusion: Agmatine causes rat bladder relaxation by activation of the I2 IR, which opens KATP channels through the cyclic AMP/protein kinase A pathway. Agmatine-induced bladder relaxation in STZ-diabetic rats is increased due to a higher expression of IR.",
author = "Tsai, {Tsung Chin} and Lin, {Chia Ho} and Chung, {Hsien Hui} and Cheng, {Juei Tang} and I-Hung Chen and Yat-Ching Tong",
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Urinary bladder relaxation through activation of imidazoline receptors induced by agmatine is increased in diabetic rats. / Tsai, Tsung Chin; Lin, Chia Ho; Chung, Hsien Hui; Cheng, Juei Tang; Chen, I-Hung; Tong, Yat-Ching.

In: LUTS: Lower Urinary Tract Symptoms, Vol. 6, No. 2, 01.01.2014, p. 117-123.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Urinary bladder relaxation through activation of imidazoline receptors induced by agmatine is increased in diabetic rats

AU - Tsai, Tsung Chin

AU - Lin, Chia Ho

AU - Chung, Hsien Hui

AU - Cheng, Juei Tang

AU - Chen, I-Hung

AU - Tong, Yat-Ching

PY - 2014/1/1

Y1 - 2014/1/1

N2 - Objectives: The effect of agmatine on bladder contractility and the diabetes-induced alteration of this action were studied in the rat. Methods: Bladder strips were isolated from 9-week-old streptozotocin (STZ)-diabetic rats and control Wistar rats. Strips were hung in an organ bath for measurement of isometric tension and pre-contracted with either 1μmol/L acetylcholine (ACh) or 50mmol/L KCl. Dose-dependent relaxation of the bladder strips was studied by cumulative administration of agmatine 1-100μmol/L into the organ bath. Effects of specific imidazoline receptor (IR) antagonists on the agmatine-induced relaxation were studied. Western blotting analysis was used to measure bladder IR, sulphonylurea receptor (SUR) and inwardly rectifying K+ channel subunit 6.2 (Kir 6.2) protein levels. Results: Agmatine reduced ACh and KCl pre-contracted bladder strip tension in a dose-dependent fashion. Relaxation was significantly increased in STZ-diabetic rats. The relaxation was inhibited by BU224, a selective I2 IR antagonist; but not by efaroxan (I1 IR antagonist) or KU14R (I3 IR antagonist). Moreover, the agmatine-induced relaxation was attenuated by glibenclamide (inhibitor of KATP channel) and H-89 (inhibitor of protein kinase A), but enhanced by 3-isobutyl-1-methylxanthine (IBMX, inhibitor of cyclic AMP phosphodiesterase). Western blotting showed increased expression of bladder IR but not SUR or Kir 6.2 in the STZ-diabetic rat. Conclusion: Agmatine causes rat bladder relaxation by activation of the I2 IR, which opens KATP channels through the cyclic AMP/protein kinase A pathway. Agmatine-induced bladder relaxation in STZ-diabetic rats is increased due to a higher expression of IR.

AB - Objectives: The effect of agmatine on bladder contractility and the diabetes-induced alteration of this action were studied in the rat. Methods: Bladder strips were isolated from 9-week-old streptozotocin (STZ)-diabetic rats and control Wistar rats. Strips were hung in an organ bath for measurement of isometric tension and pre-contracted with either 1μmol/L acetylcholine (ACh) or 50mmol/L KCl. Dose-dependent relaxation of the bladder strips was studied by cumulative administration of agmatine 1-100μmol/L into the organ bath. Effects of specific imidazoline receptor (IR) antagonists on the agmatine-induced relaxation were studied. Western blotting analysis was used to measure bladder IR, sulphonylurea receptor (SUR) and inwardly rectifying K+ channel subunit 6.2 (Kir 6.2) protein levels. Results: Agmatine reduced ACh and KCl pre-contracted bladder strip tension in a dose-dependent fashion. Relaxation was significantly increased in STZ-diabetic rats. The relaxation was inhibited by BU224, a selective I2 IR antagonist; but not by efaroxan (I1 IR antagonist) or KU14R (I3 IR antagonist). Moreover, the agmatine-induced relaxation was attenuated by glibenclamide (inhibitor of KATP channel) and H-89 (inhibitor of protein kinase A), but enhanced by 3-isobutyl-1-methylxanthine (IBMX, inhibitor of cyclic AMP phosphodiesterase). Western blotting showed increased expression of bladder IR but not SUR or Kir 6.2 in the STZ-diabetic rat. Conclusion: Agmatine causes rat bladder relaxation by activation of the I2 IR, which opens KATP channels through the cyclic AMP/protein kinase A pathway. Agmatine-induced bladder relaxation in STZ-diabetic rats is increased due to a higher expression of IR.

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