THE DECOMPENSATED DETRUSOR .2. EVIDENCE FOR LOSS OF SARCOPLASMIC-RETICULUM FUNCTION AFTER BLADDER OUTLET OBSTRUCTION IN THE RABBIT

Purpose: While it may lack the classic morphological pattern in striat ed muscle systems, there is ample evidence that smooth muscle also con tains sarcoplasmic reticulum. These intracellular storage sites releas e calcium into the cytosol to generate contractile force in response t o various stimuli. A major component of the sarcoplasmic reticulum is an adenosine triphosphate dependent ion pump, which serves to drive fr ee calcium out of the cytosol back into this intracellular reservoir. This ion pump serves to maintain the intracellular calcium storage sit es, 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 obstructi ons) based on physiological performance. These were correlated with bi ochemical and molecular determinations of sarcoplasmic endoplasmic ret iculum calcium, magnesium-adenosinetriphosphatase expression. Results: Our results demonstrate a remarkable loss of sarcoplasmic endoplasmic reticulum calcium-adenosinetriphosphatase activity in the decompensat ed group and a moderate loss in the compensated group. Conclusions: Th ese data provide molecular support for our previous physiological stud ies in which we demonstrated an important role for intracellular calci um storage and release with normal bladder smooth muscle function. The se data strongly support our contention that contractile dysfunction i n bladder smooth muscle following outlet obstruction is partially medi ated by changes in the mechanisms of intracellular calcium homeostasis .