The Decompensated Detrusor II: Evidence for Loss of Sarcoplasmic Reticulum Function After Bladder Outlet Obstruction in the Rabbit

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Abstract
Purpose: While it may lack the classic morphological pattern in striated muscle systems, there is ample evidence that smooth muscle also contains sarcoplasmic reticulum. These intracellular storage sites release calcium into the cytosol to generate contractile force in response to various stimuli. A major component of the sarcoplasmic reticulum is an adenosine triphosphate dependent ion pump, which serves to drive free calcium out of the cytosol back into this intracellular reservoir. This ion pump serves to maintain the intracellular calcium storage sites, and also as a marker of the sarcoplasmic reticulum. Materials and Methods: Muscle strip studies were performed to stratify the data into 3 major groups (controls, and compensated and decompensated obstructions) based on physiological performance. These were correlated with biochemical and molecular determinations of sarcoplasmic endoplasmic reticulum calcium, magnesium-adenosinetriphosphatase expression. Results: Our results demonstrate a remarkable loss of sarcoplasmic endoplasmic reticulum calcium-adenosinetriphosphatase activity in the decompensated group and a moderate loss in the compensated group. Conclusions: These data provide molecular support for our previous physiological studies in which we demonstrated an important role for intracellular calcium storage and release with normal bladder smooth muscle function. These data strongly support our contention that contractile dysfunction in bladder smooth muscle following outlet obstruction is partially mediated by changes in the mechanisms of intracellular calcium homeostasis.