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Enhanced ATP release from rat bladder urothelium during chronic bladder inflammation: effect of botulinum toxin A.
Neurochem Int. 2005 Sep; 47(4):291-7.NI

Abstract

The effects of mechanoreceptor stimulation and subsequent ATP release in cyclophosphamide evoked chronic bladder inflammation was examined to demonstrate: (1) whether inflammation modulates ATP release from bladder urothelium and (2) whether intravesical botulinum toxin A administration inhibits urothelial ATP release, a measure of sensory nerve activation. ATP release was measured from rat bladders in a Ussing chamber, an apparatus that allows one to separately measure resting and mechanoreceptor evoked (e.g. hypoosmotic stimulation) ATP release from urothelial and serosal sides of the bladder. Cystometry was utilized to correlate changes in ATP release with alterations in the frequency of voiding and non-voiding bladder contractions, in vivo measures of bladder afferent activity. The resting urothelial release of ATP was not significantly affected by either cyclophosphamide or botulinum toxin A treatment. However, evoked ATP release following hypoosmotic stimulation was significantly increased (i.e. 94%) in chronic cyclophosphamide treated bladder urothelium compared to control bladders. In addition, botulinum toxin A treatment significantly reduced hypoosmotic shock induced ATP release in cyclophosphamide treated animals by 69%. Cystometry revealed that cyclophosphamide and botulinum toxin A treatments altered non-voiding (i.e. cyclophosphamide increased, botulinum toxin A decreased) but not voiding contraction frequency suggesting that alterations in urothelial ATP release selectively diminished underlying bladder C-fiber nerve activity. Finally, intravesical instillation of botulinum toxin A did not affect ATP release from the serosal side implying that its effects were confined to the urothelial side of the bladder preparation.

Authors+Show Affiliations

Scott Department of Urology, Baylor College of Medicine, One Baylor Plaza, Alkek N720, Houston, TX 77030, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

15970360

Citation

Smith, Christopher P., et al. "Enhanced ATP Release From Rat Bladder Urothelium During Chronic Bladder Inflammation: Effect of Botulinum Toxin A." Neurochemistry International, vol. 47, no. 4, 2005, pp. 291-7.
Smith CP, Vemulakonda VM, Kiss S, et al. Enhanced ATP release from rat bladder urothelium during chronic bladder inflammation: effect of botulinum toxin A. Neurochem Int. 2005;47(4):291-7.
Smith, C. P., Vemulakonda, V. M., Kiss, S., Boone, T. B., & Somogyi, G. T. (2005). Enhanced ATP release from rat bladder urothelium during chronic bladder inflammation: effect of botulinum toxin A. Neurochemistry International, 47(4), 291-7.
Smith CP, et al. Enhanced ATP Release From Rat Bladder Urothelium During Chronic Bladder Inflammation: Effect of Botulinum Toxin A. Neurochem Int. 2005;47(4):291-7. PubMed PMID: 15970360.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Enhanced ATP release from rat bladder urothelium during chronic bladder inflammation: effect of botulinum toxin A. AU - Smith,Christopher P, AU - Vemulakonda,Vijaya M, AU - Kiss,Susanna, AU - Boone,Timothy B, AU - Somogyi,George T, PY - 2005/01/07/received PY - 2005/04/10/revised PY - 2005/04/11/accepted PY - 2005/6/23/pubmed PY - 2005/9/9/medline PY - 2005/6/23/entrez SP - 291 EP - 7 JF - Neurochemistry international JO - Neurochem Int VL - 47 IS - 4 N2 - The effects of mechanoreceptor stimulation and subsequent ATP release in cyclophosphamide evoked chronic bladder inflammation was examined to demonstrate: (1) whether inflammation modulates ATP release from bladder urothelium and (2) whether intravesical botulinum toxin A administration inhibits urothelial ATP release, a measure of sensory nerve activation. ATP release was measured from rat bladders in a Ussing chamber, an apparatus that allows one to separately measure resting and mechanoreceptor evoked (e.g. hypoosmotic stimulation) ATP release from urothelial and serosal sides of the bladder. Cystometry was utilized to correlate changes in ATP release with alterations in the frequency of voiding and non-voiding bladder contractions, in vivo measures of bladder afferent activity. The resting urothelial release of ATP was not significantly affected by either cyclophosphamide or botulinum toxin A treatment. However, evoked ATP release following hypoosmotic stimulation was significantly increased (i.e. 94%) in chronic cyclophosphamide treated bladder urothelium compared to control bladders. In addition, botulinum toxin A treatment significantly reduced hypoosmotic shock induced ATP release in cyclophosphamide treated animals by 69%. Cystometry revealed that cyclophosphamide and botulinum toxin A treatments altered non-voiding (i.e. cyclophosphamide increased, botulinum toxin A decreased) but not voiding contraction frequency suggesting that alterations in urothelial ATP release selectively diminished underlying bladder C-fiber nerve activity. Finally, intravesical instillation of botulinum toxin A did not affect ATP release from the serosal side implying that its effects were confined to the urothelial side of the bladder preparation. SN - 0197-0186 UR - https://www.unboundmedicine.com/medline/citation/15970360/Enhanced_ATP_release_from_rat_bladder_urothelium_during_chronic_bladder_inflammation:_effect_of_botulinum_toxin_A_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0197-0186(05)00113-0 DB - PRIME DP - Unbound Medicine ER -