Hyperreflexia, a condition characterized by contractions of the urinary bladder, is not mediated by a micturition reflex. The contractions can be of neurogenic origin through spinal or supraspinal reflexes or of myogenic origin, independent of neuronal mediation. There is a clear relationship between hyperreflexia and symptoms such as urgency, frequency, nocturia and urinary incontinence. Therapies to reduce the presence of uninhibited bladder contractions include oral drug therapy, instillation drug therapy and parasympathetic nerve ablation. The current study characterizes the ability of terodiline to inhibit an experimental form of hyperreflexia and compares the efficacy and potency of terodiline and other agents on hyperreflexia and evoked contractions. The results can be summarized as follows: (1) terodiline inhibits the amplitude of the hyperreflexia at lower concentrations than it inhibits the frequency of hyperreflexia; (2) terodiline had no statistically significant effect on mean blood pressure at any concentration utilized; (3) terodiline had approximately the same potency for inhibition of 2 and 32 Hz stimulation for both the bladder body and base; (4) terodiline inhibited the maximum contractile response to bethanechol and also shifted the curve to the right, demonstrating that terodiline is a mixed inhibitor, and (5) terodiline was a noncompetitive inhibitor of KCI.

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