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1 Surgery, Chinese University of Hong Kong, New Territories, Pennsylvania, Hong Kong
2 Pharmacology, University of Pittsburgh, Pittsburgh, Pennsylvania, United States
3 Pediatric Urology, Children's Hospital of Pittsburgh, Pittsburgh, Pennsylvania, United States
* To whom correspondence should be addressed. E-mail: wuhy{at}chp.edu.
In vitro preparations of whole urinary bladders of neonatal rats exhibit prominent myogenic spontaneous contractions, the amplitude and frequency of which can be increased by muscarinic agonists. The muscarinic receptor subtype responsible for this facilitation was examined in the present experiments. Basal spontaneous contractions in 1-2 week old Sprague - Dawley rat bladders were not affected by M2 or M3 antagonists. However administration of physostigmine (0.5 µM), an anticholinesterase agent that increases the levels of endogenous acetylcholine, or carbachol (50-100 nM), a cholinergic agonist at low concentrations which did not cause tonic contractions, significantly augmented the frequency and amplitude of spontaneous contractions. Blockade of M2 receptors with AF-DX 116 (0.1 µM) or methoctramine (1µM), or blockade of M3 receptors with 4-DAMP (50 nM) or 4-DAMP mustard (0.1 µM) reversed the physostigmine and carbachol responses. M2 and M3 blockade did not alter the facilitation of spontaneous contractions induced by Bay K-8644 (10 nM), an L-type calcium channel opener, or iberiotoxin (0.1 µM), a BKCa channel blocker. NS1619 (30 µM), a BKCa channel opener, decreased carbachol augmented spontaneous contractions. These results suggest that spontaneous contractions in the neonatal rat bladder are enhanced by activation of both M2 and M3 receptors by endogenous acetylcholine released in the presence of an anticholinesterase agent or a cholinergic receptor agonist.
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