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- W2003193484 abstract "OBJECTIVE To study the involvement of extracellular Ca 2+ and the properties of the intracellular Ca 2+ ([Ca 2+ ] i ) stores on the carbachol‐induced contraction of mammalian urinary bladder smooth muscle strips under polarized and depolarized conditions. MATERIALS AND METHODS Strips of bladder were suspended between platinum ring electrodes in a cylindrical organ bath (0.2 mL) and continuously superfused with Krebs’ solution at 1 mL/min. The effect of nifedipine, cyclopiazonic acid (CPA), thapsigargin, procaine, ryanodine and caffeine before and during a 10‐s application of 100 µ m carbachol under polarized conditions were studied. The effect of these drugs was also assessed under depolarized conditions using a protocol that allowed a more detailed assessment of the role of [Ca 2+ ] i stores, consisting of emptying the stores by exposure to Ca 2+ ‐free solution, rapidly refilling them by a 10‐s application of 81.5 m m Ca 2+ (priming), returning to the Ca 2+ ‐free solution for 3 min and then applying 100 µ m carbachol (10 s) in Ca 2+ ‐free solution (store release). RESULTS Under polarized conditions, nifedipine and Ca 2+ removal almost completely inhibited the carbachol‐induced contractions. CPA increased the amplitude and duration of both carbachol‐ and electrical field stimulation‐induced contractions. Although ryanodine had no inhibitory effect, caffeine and procaine significantly inhibited the carbachol‐induced contraction. Under depolarized conditions nifedipine blocked both priming and store release contractions. CPA, thapsigargin, procaine and ryanodine significantly increased the priming and inhibited the store release contractions. However, caffeine virtually abolished both priming and store release contractions. CONCLUSION These results suggest that in guinea‐pig urinary bladder smooth muscle the Ca 2+ necessary for contraction enters the cell through voltage‐dependent dihydropiridine‐sensitive Ca 2+ channels and is pumped into an intracellular store that is released by carbachol. Under polarized conditions, the blockade of sarco‐endoplasmic reticulum calcium ATP‐ase (SERCA) with CPA increases [Ca 2+ ] i and carbachol‐induced contractions. The effects of caffeine and procaine suggest that store release involves ryanodine receptors and calcium‐induced calcium release. Under depolarized conditions, Ca 2+ entry is blocked by nifedipine and the stores diminish. Stored Ca 2+ is also greatly reduced by the blockade of SERCA with either CPA or thapsigargin. Procaine, ryanodine and caffeine blocked the store release contractions, suggesting that this involves ryanodine receptors and calcium‐induced calcium release." @default.
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- W2003193484 date "2006-09-05" @default.
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- W2003193484 title "The role of Ca<sup>2+</sup>influx and intracellular Ca<sup>2+</sup>release in the muscarinic-mediated contraction of mammalian urinary bladder smooth muscle" @default.
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- W2003193484 doi "https://doi.org/10.1111/j.1464-410x.2006.06431.x" @default.
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