The influence of bladder outflow obstruction on the peripheral nervous control of the detrusor was investigated in female rats. The obstruction was performed by means of partial urethral ligation. The influence of exogenously applied drugs and electrical field stimulation was investigated after obstruction for 6 weeks. The content of noradrenaline and choline acetyltransferase was also determined as well as the density of alpha-adrenoceptors. A significant decrease of the contractile response to alpha-adrenoceptor stimulation was found in the obstructed bladders when compared to normal controls. Also the density of alpha-adrenoceptors decreased in the obstructed bladders. The concentrationresponse relationship to carbachol remained unchanged, and neither were any changes seen in the relation between the cholinergic and noncholinergic components of the electrically induced, nerve-mediated contractile response. A rightward shift of the frequencyresponse curve for the obstructed bladders was found with 50% of the maximum response occurring at 13 Hz compared to 4 Hz in the control preparations. The total amount of both noradrenaline and choline acetyltransferase had increased after 6 weeks of obstruction, but owing to the pronounced degree of hypertrophy of the bladder wall the concentrations were only approximately 30% of those in the control bladders, which also was the case after 1 and 3 weeks of obstruction.
It is concluded that changes in the peripheral nervous control of the rat bladder seem to occur secondary to outflow obstruction, but also that some of the changes observed might be due to factors unrelated to innervation and receptor-mediated functions. Whether the decreased alpha-adrenoceptor mediated influence seen in the presence of obstruction might reflect a generally decreased adrenergic influence in the obstructed bladder remains to be established.