Extracellular electrical signals, free from the artifacts that have plagued electromyographic (EMG) recordings from detrusor smooth muscle, have been recorded from a whole guinea-pig bladder preparation using suction electrodes (Ballaro et al. 2001). Here we characterise the signal recorded from mucosa-free detrusor strips, a preparation more readily superfused with pharmacological agents.

Mucosa-free detrusor strips (3 X 10 mm) were dissected from the bladders of male (300-500 g) Dunkin Hartley guinea-pigs that had been killed by cervical dislocation using Schedule 1 methods. Strips were superfused with Tyrode solution (35 ± 1 °C), attached to a pressure transducer and electrically stimulated by 2-6 pulses (0.1 ms) via a tripolar electrode. Electrical signals recorded using a bipolar reversible (Pt/PtCl) suction electrode sucked onto the exposed surface of the detrusor strip were processed and displayed in real time with changes in strip tension. The sensitivities of α, β-methylene ATP (α, β-MA, 10-100 µM), and Ca²⁺ channel blockers nifedipine (30 µM) plus NiCl₂ (0.5 mM), or CdCl₂ (20 µM) were determined.

An electrical signal, with parameters (mean ± S.D.): amplitude 222 ± 238 µs, duration 236 ± 139 ms, time to maximum depolarisation 43 ± 16 ms, was consistently recorded from 37 detrusor strips taken from 24 animals. The signal was sensitive to graded reduction in [CaCl₂] of the superfusate, and was abolished by solutions containing < 0.4 mM CaCl₂ (n = 6), and TTX (1 µM) (n = 7). The signal was abolished by α, β-MA in association with an attenuated contraction (n = 12). With atropine, in four strips the electrical signal was unchanged despite a significant reduction in tension (78 ± 6 % of control, P < 0.01, Student’s t test); however, in three the signal was reduced to 62 ± 8 % of control. Signal amplitude was reduced to 18 ± 9 % of control (n = 6) in the presence of nifedipine and NiCl₂, and to 9 ± 3 % of control (n = 4) by nifedipine and CdCl₂; the contraction was abolished. In two experiments the residual electrical signal was abolished by α, β-MA.

Extracellular reflections of smooth muscle depolarisation can be recorded, isolated from stimulus artifact, and correlated with tension generated by nerve stimulation, from guinea-pig detrusor strips using reversible suction electrodes. We confirm the implications of previous studies (Fujii, 1988) in demonstrating that the electrical signal originates primarily from a purinergic mechanism, although it may also contain an atropine-sensitive component. Provided that the electrophysiological basis of neurotransmission in man and guinea-pig is similar, the experimental set-up presented here will be a valuable tool to investigate in vitro, and clinically by electro-myography, the pathological purinergic neuro-transmission that can be expressed in addition to normal cholinergic mechanisms, in detrusor samples taken from dysfunctional human bladders.

This study was funded by a University College London Hospitals fast track grant.