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Bladder outlet obstruction induces marked morphological, functional, and metabolic changes within the urinary bladder. Recent studies indicate that there is a close correlation between the contractile dysfunction induced by partial outlet obstruction and a marked decrease in mitochondrial oxidative activity of the hypertrophied bladder tissue. The current study investigates the effect of partial outlet obstruction on adenine metabolism within the bladder tissue. After transport into the cell, adenine becomes available as a substrate for adenine phosphoribosyl transferase (APRT), the enzyme that catalyses the non-mitochondrial conversion of adenine into AMP. Subsequently, AMP is phosphorylated to ADP, the phosphate acceptor in mitochondrial oxidative phosphorylation. The results of these studies demonstrate that partial outlet obstruction induces a significant increase in 14C-adenine uptake into the urinary bladder smooth muscle which in turn provides substrate for APRT and results in an increase in 14C-AMP synthesis. In contrast, the rate of incorporation of adenine into ATP+ADP was similar for both control and obstructed tissue. The activity of APRT was not significantly different in control and obstructed tissue.
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Haugaard et al. (1993) studied this question.
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