Atropine-resistant transmission in partially depolarized rat urinary bladder

1. Phasic contractile responses of the intact rat urinary bladder to the muscarinic agonists carbachol and pilocarpine became nearly blocked as the concentrations were progressively increased to 200-500 microM. In contrast, tonic contractile responses remained elevated throughout progressive increases in agonist concentration. 2. Nerve-induced phasic contractions to 1 Hz stimuli were potentiated throughout progressive increases in the concentration of muscarinic agonists. However, these responses were more atropine sensitive than untreated controls and responses to 1 Hz stimuli were nearly abolished. 3. After inhibition of cholinesterase, the action of cholinergic transmitter released during prolonged nerve stimulation may extend to the tonic contractile state of the bladder and potentiate responses to 1H stimuli. Nerve-induced responses were more atropine sensitive than untreated controls. 4. Bladder tone was increased and nerve-induced contractions to 1-Hz stimuli were also potentiated in an elevated K+ environment. However, atropine sensitivity of nerve-induced responses w s reduced. 5. Nerve-induced bladder contractions were linked to the tonic contractile state of the bladder muscle, controlled physiologically by muscarinic receptors. Since phasic contractile responses to muscarinic agonists were abolished at high concentrations by receptor desensitization, nerve-induced responses must be elicited under these conditions by a non-cholinergic transmitter.