Abstract

1 Strips of urethra taken from guinea-pigs contracted in response to acetylcholine, noradrenaline (via alpha-adrenoceptors) and 5-hydroxytryptamine, and were relaxed by adenosine triphosphate (ATP) if the tone was raised. Isoprenaline produced relaxation of bladder strips (via beta-adrenoceptors) whereas ATP caused contraction. 2 Atropine completely blocked all responses to acetylcholine; quinidine failed to block ATP responses selectively; methysergide blocked responses of the urethra but not the bladder to 5-hydroxytryptamine. 3 Spontaneous electrical activity was recorded with intracellular microelectrodes from all regions: in the urethra infrequent bursts of spikes occurred at 1-7 min intervals; regular spikes at 6-30/min were recorded from the detrusor muscle. In the bladder base, bursts of spikes were superimposed on the regular pattern. 4 Bursts of spikes in the urethra were initiated by noradrenaline, phenylephrine or acetylcholine and inhibited by ATP; regular spikes in the bladder were accelerated by acetylcholine or ATP and slowed by noradrenaline or isoprenaline. 5 The intrinsic electrical activity and pharmacological properties of the urethra therefore differ from those of the bladder. This may account for the different responses of the two regions in normal function.

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