The Journal of Urology · 1996 · 17 citations · 5 references
Life SciencesPhysiologyUrologyCalcium HomeostasisIntracellular TransportSignal TransductionBladder DysfunctionBladder Outlet ObstructionCalcium MetabolismCalcium SignalingIntracellular Calcium SignalingLower Urinary Tract PhysiologyBladder Outlet Obstruction Effects On Detrusor FunctionCalcium Release From Intracellular StoresCalcium TransportDetrusor Calcium HandlingIntracellular Calcium DynamicsIntracellular Calcium HomeostasisIntracellular Calcium ReleaseUrinary Calcium Handling
No AccessJournal of UrologyBladder Research1 Aug 1996The Decompensated Detrusor I: The Effects of Bladder Outlet Obstruction on the Use of Intracellular Calcium Stores Dorothea Rohrmann, Robert M. Levin, John W. Duckett, and Stephen A. Zderic Dorothea RohrmannDorothea Rohrmann , Robert M. LevinRobert M. Levin , John W. DuckettJohn W. Duckett , and Stephen A. ZdericStephen A. Zderic View All Author Informationhttps://doi.org/10.1016/S0022-5347(01)65756-2AboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookLinked InTwitterEmail Abstract Purpose: As in other smooth muscle groups, extracellular calcium influx as well as the release of calcium from intracellular storage sites or sarcoplasmic reticulum occur in response to receptor stimulation. The relative participation of extracellular influx versus intracellular release has recently been shown to be influenced by developmental stage and obstruction. Partial bladder outlet obstruction results in marked hypertrophy of the bladder and produces alterations in contractile function. To understand better how this contractile dysfunction after outlet obstruction is influenced by intracellular calcium handling we tested the effects of 2 drugs with known effects on the sarcoplasmic reticulum. Materials and Methods: We evaluated ryanodine, which blocks the release of calcium from the sarcoplasmic reticulum, and thapsigargin, which blocks the ability of the sarcoplasmic reticulum to pump cytosolic calcium back into the storage sites. Rabbit bladders were obstructed for different periods, after which detrusor muscle strips were harvested and contractile performance was evaluated in the absence and presence of ryanodine and thapsigargin. Results: In the early phases of outlet obstruction the release of intracellular calcium increased significantly. With prolonged obstruction and detrusor decompensation the intracellular storage sites lost the ability to contribute to the generation of contractile force. Conclusions: Alterations in the calcium handling ability of the smooth muscle cell appear to have an important role in the process of decompensation of bladder function in infravesical obstruction. References 1 : Receptor operated intracellular calcium stores in the smooth muscle of the guinea pig bladder. J. Urol.1985; 133: 900. Link, Google Scholar 2 : Developmental aspects of excitation contraction coupling of rabbit bladder smooth muscle. J. Urol., part 21994; 152: 679. Abstract, Google Scholar 3 : Developmental aspects of excitation contraction coupling in bladder smooth muscle. In: Muscle, Matrix and Bladder Function. Edited by . New York: Plenum Press1995: 105. Google Scholar 4 : Ontogeny of the ryanodine receptor in rabbit urinary bladder smooth muscle. Molec. Cell. Biochem.1994; 137: 169. Google Scholar 5 : Excitation contraction coupling and the ultrastructure of smooth muscle. Circ. Res.1985; 57: 497. Google Scholar 6 Berridge, M. J., Cheek, T. R., Bennett, D. and Bootman, M. D.: Ryanodine receptors and intracellular signaling. In: Ryanodine Receptors. Edited by V. Sorrentino. CRC Press, in press. Google Scholar 7 : Ryanodine receptors: how many, where and why?. Trends Pharm. Sci.1993; 14: 98. Google Scholar 8 : Thapsigargin, a novel molecular probe for studying intracellular calcium relase and storage. Agents Actions1989; 27: 17. Google Scholar 9 Zderic, S. A., Rohrmann, D., Gong, C., Snyder, H. McC., Duckett, J. W., Wein, A. J. and Levin, R. M.: The decompensated detrusor II: evidence for loss of sarcoplasmic reticulum function following bladder outlet obstruction in the rabbit. J. Urol., in press. Google Scholar 10 : Pathophysiology of cardiac hypertrophy and failure of human myocardium: abnormalities of calcium handling. In: Cellular and Molecular Alterations in the Failing Human Heart. Edited by . New York: Springer Verlag1992. Google Scholar 11 : Selective changes in cardiac gene expression during compensated hypertrophy and the transition to cardiac decompensation in rats with chronic aortic banding. Circ. Res.1993; 73: 184. Google Scholar From the Department of Urology, Children's Hospital of Philadelphia and Division of Urology, University of Pennsylvania, School of Medicine and Veteran's Medical Center, Philadelphia, Pennsylvania.© 1996 by American Urological Association, Inc.FiguresReferencesRelatedDetailsCited byLEMACK G, BURKHARD F, ZIMMERN P, MCCONNELL J and LIN V (2018) PHYSIOLOGIC SEQUELAE OF PARTIAL INFRAVESICAL OBSTRUCTION IN THE MOUSE: ROLE OF INDUCIBLE NITRIC OXIDE SYNTHASEJournal of Urology, VOL. 161, NO. 3, (1015-1022), Online publication date: 1-Mar-1999. Volume 156Issue 2SAugust 1996Page: 578-581 Advertisement Copyright & Permissions© 1996 by American Urological Association, Inc.MetricsAuthor Information Dorothea Rohrmann More articles by this author Robert M. Levin More articles by this author John W. Duckett More articles by this author Stephen A. Zderic More articles by this author Expand All Advertisement PDF downloadLoading ...
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Arthur M. Feldman, Ellen O. Weinberg, Phillip E. Ray et al. · Circulation Research · 1993 · 355 citations · Full text