Transmitters contributing to the voiding contraction in female rats

To assess in detail the contribution of acetylcholine and ATP to the different phases of the voiding contraction, urine flow and rhabdosphincter electromyographic (RB-EMG) activity in rats, using alpha,beta-methylene-ATP (desensitizing purinoceptors) and atropine (blocking muscarinic receptors). These agents and possibly other transmitters contribute to bladder emptying in rats, but how they contribute to the different phases of the micturition cycle, including the intraluminal pressure high-frequency oscillations (IPHFOs) is unclear.

Adult anaesthetized female Sprague-Dawley rats were used; intravesical pressure, RB-EMG and urine flow from the distal urethra were recorded. After baseline recordings, alpha,beta-methylene-ATP (0.5 mg/kg), atropine (1 mg/kg), or both, were injected intravenously.

Alpha,beta-Methylene-ATP significantly decreased the maximum bladder pressure during the first micturition phase, whereas atropine had little effect; the maximum bladder pressure during the second phase was also reduced. IPHFOs were apparent after both treatments. Atropine significantly reduced the maximum bladder pressure during the third phase. The maximum urinary flow rate was reduced by both alpha,beta-methylene-ATP and atropine; after exposure to both agents together, urinary flow was markedly reduced or stopped, and overflow incontinence developed.

ATP contributes mainly to the initial and acetylcholine to the later phases of the voiding cycle in the rat. Neither agent abolished the IPHFOs; even after blocking the receptors for one transmitter and in the presence of IPHFOs, the bladder can still empty. However, if both receptors are blocked, overflow incontinence develops, suggesting that even if further transmitters are taking part in the voiding contraction, their physiological significance is questionable.