Contractile proteins and their response to bladder outlet obstruction.

Abstract

Urinary outlet obstruction causes rapid increases in bladder mass; the extent of the increase in mass is directly proportional to the severity of the obstruction1–3. Although there may be some species differences, in general, the changes in bladder contractility associated with outlet obstruction are also dependent upon the degree of increase in bladder mass. Bladder strips from animals with “mild” obstruction (less than 3-fold increase in bladder mass) respond to electrical field stimulation or contractile agents with no change or increases in contractile response compared to controls1–5. In contrast, bladder strips from animals with “severe” obstruction, where the bladder mass increases more than 6-fold, respond to contractile stimuli with decreases in contractile responses and an impaired ability of the bladder to empty2,3,6–10. Depending on the duration and severity of obstruction, removal of the obstruction generally causes reversal of the contractile dysfunction11,12. The mechanisms responsible for the changes in bladder contractility associated with bladder outlet obstruction are still unclear, but as described in other chapters in this book, may include alterations in glucose metabolism13–19, in bladder innervation and/or action potential properties20–25, or alterations in the contractile proteins responsible for smooth muscle contraction26–31. The latter mechanism will be discussed in this chapter.