[Acceleration of ATP-induced contraction in the obstructed bladder of the rat]

Detrusor instability is one of the most common problems in patients with lower urinary tract obstructive diseases, such as benign prostatic hyperplasia. Adenosine triphosphate (ATP) has been associated as a neuronal component in the detrusor instability.

Ninety-six female Splague-Dawley rats were studied. Outflow obstructions were created by ligature of the urethra over which a catheter was placed. Changes in the bladder capacity, and an isovolumetric contractile response to pharmacologic antagonists were studied in the obstructed rats for a period of from one day to four weeks.

The bladder capacity of rats obstructed for four weeks increased significantly. Maximum bladder contraction pressure with the use of atropine medication was inhibited in 60 percent and, 30 percent of in the control group, respectively. The inhibitory effect of the maximum bladder contraction pressure by the pyridoxalphosphate-6-azophenyl-2', 4'-disulphonate (PPADS) dosage after the atropine dosage was not recognized it in the control group, but the effect was recognized powerfully in the obstructed group.

In the obstructed bladder rat, strong rise of the bladder contraction by P2X receptor with a lower urinary obstruction was accepted, and that result reflects positively. Therefore, it was guessed that the result was an end of the compensatory mechanism of unstable bladder.