Intracellular Ca(2+) regulation and electrophysiolgical properties of bladder urothelium subjected to stretch and exogenous agonists.
Wu, C, Gui, GP and Fry, CH (2011) Intracellular Ca(2+) regulation and electrophysiolgical properties of bladder urothelium subjected to stretch and exogenous agonists. Cell Calcium, 49 (6). 395 - 399. ISSN 0143-4160
Intracellular Ca(2+) control and the electrophysiological properties of guinea-pig urothelium were measured during interventions encountered during bladder filling, including cell stretch and exposure to exogenous transmitters such as ATP and muscarinic agonists. Stretch, achieved by exposure to solutions of altered osmolality, generated intracellular Ca(2+)-transients that were attenuated by Gd(3+) in isolated cells. However ATP-induced intracellular Ca(2+)-transients were unaffected by Gd(3+) but blocked by thapsigargin. ATP-dependent Ca(2+)-transients were followed by a large inward current at a holding potential of -60mV. Carbachol was without significant effect, except for a small slowing of the rate of spontaneous intracellular Ca(2+)-transients that were recorded in about one-third of cells. With urothelial sheets the transepithelial potential (TEP) was increased by ATP applied to the baso-lateral (serosal) face, a similar change was achieved by reduction of the basolateral [Na]; carbachol was without significant effect. We propose that a rise of intracellular Ca(2+) may control ATP release as both mechanical stretch and exogenous ATP have been shown previously to release further ATP from isolated urothelium as part of a postulated signalling pathway for bladder filling. The similar increase of TEP by ATP and a raised transepithelial Na gradient is also consistent with a role for transepithelial ion transport as a regulator of ATP release. The lack of large effects with carbachol implies muscarinic agonists must exert any effects on the urothelium through other pathways.
|Additional Information:||NOTICE: This is the author’s version of a work that was accepted for publication in Cell Calcium. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in Cell Calcium, 49(6), June 2011, DOI 10.1016/j.ceca.2011.03.008.|
|Divisions:||Faculty of Health and Medical Sciences > Biochemistry and Physiology|
|Depositing User:||Symplectic Elements|
|Date Deposited:||26 Mar 2012 14:54|
|Last Modified:||23 Sep 2013 19:05|
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