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. Author manuscript; available in PMC: 2009 Oct 12.
Published in final edited form as: Am J Physiol Renal Physiol. 2008 Jan 23;294(4):F821–F829. doi: 10.1152/ajprenal.00321.2006

Figure 2. UTP and UTPγS evoked changes in intracellular calcium in cultured rat urothelial cells are significantly attenuated by inhibition of the SERCA pump and phospholipase C.

Figure 2

(A) and (D) illustrate UTP (10 μM) and UTPγS (10 μM) evoked changes in [Ca2+]i normal physiological calcium (2 mM). (B) and (E) in the absence of extracellular calcium, the amplitude of UTP (10 μM) and UTPγS (10 μM) evoked responses were not significantly different that those in normal extracellular calcium. (C) and (F) thapsigargin (10 μM) was used to deplete intracellular calcium stores by inhibiting the SERCA pump. Both UTP (10 μM) and UTPγS (10 μM) responses were abolished under these conditions. (G) and (H) Pre-treatment of rat urothelial cells with the PLC inhibitor, U73122 (10 μM) significantly attenuated both UTP (10 μM) and UTPγS (10 μM) evoked changes in [Ca2+]i. (I) Histograms illustrating the mean changes in [Ca2+]i evoked by UTP (10 μM) and UTPγS (10 μM) as a percentage of the maximum ionomycin (5 μM) response in rat urothelial cells alone and following pre-treatment with thapsigargin (10 μM) and U73122 (10 μM); ** P<0.01.

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