Neurotransmission in activation of the contractile response in the human urinary bladder.

The endogenous contracting transmitter at the neuromuscular junction in strips from human urinary bladder has been investigated using field stimulation and selective antagonists. Atropine in low concentrations was found to inhibit bladder contractions whereas higher concentrations of the drug sometimes had the opposite effects. Indomethacin inhibited, phentolamine enhanced and methysergide had no dose-dependent effect on the field stimulation response. It is proposed that acetylcholine is one of the transmitter substances responsible for the contraction of the human detrusor. Species differences which could be responsible for the alleged atropine-resistance of the bladder are discussed. It is concluded that anticholinergic drugs should be of therapeutic value for treatment of muscular hyperactivity in the human urinary bladder.