Pharmacologic responses of the mouse urinary bladder

• Autorzy: A. Canda , Christopher Chapple , Russ Chess-Williams
• Języki publikacji: EN

Abstrakty

EN

The aim of the study was to determine pathways involved in contraction and relaxation of the mouse urinary bladder. Mouse bladder strips were set up in gassed Krebs-bicarbonate solution and responses to various drugs and electrical field stimulation were obtained. Isoprenaline (b-receptor agonist) caused a 63% inhibition of carbachol precontracted detrusor (EC50=2nM). Carbachol caused contraction (EC50=0.3µM), responses were antagonised more potently by 4-DAMP (M3-antagonist) than methoctramine (M2-antagonist). Electrical field stimulation caused contraction, which was inhibited by atropine (60%) and less by guanethidine and α,β-methylene-ATP. The neurogenic responses were not potentiated by inhibition of nitric oxide synthase. Presence of an intact urothelium significantly depressed responses to carbachol (p=0.02) and addition of indomethacin and L-NNA to remove prostaglandin and nitric oxide production respectively did not prevent the inhibitory effect of the urothelium. In conclusion, b-receptor agonists cause relaxation and muscarinic agonists cause contraction via the M3-receptor. Acetylcholine is the main neurotransmitter causing contraction while nitric oxide has a minor role. The mouse and human urothelium are similar in releasing a factor that inhibits contraction of the detrusor muscle which is unidentified but is not nitric oxide or a prostaglandin. Therefore, the mouse may be used as a model to study the lower urinary tract.

Słowa kluczowe

EN

Mouse; Urinary bladder; Urothelium; Contraction; Relaxation

• Czasopismo: Open Medicine
• Rocznik: 2009
• Tom: 4
• Numer: 2
• Strony: 192-197

Daty

wydano

2009-06-01

online

2009-03-27

Twórcy

autor

A. Canda

• Department of Biomedical Science, University of Sheffield, S102JF, Sheffield, UK,

autor

Christopher Chapple

• Department of Urology, The Royal Hallamshire Hospital, S102JF, Sheffield, UK

autor

Russ Chess-Williams

• Department of Biomedical Science, University of Sheffield, S102JF, Sheffield, UK

Bibliografia

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Identyfikatory

DOI

10.2478/s11536-008-0082-2