The Ewha Medical Journal
Ewha Womans University School of Medicine
Original Article

Effects of Purine Nucleotides on Motility of Urinary Bladder

Ho Sun Lee
Corresponding author: Ho Sun Lee. Department of Urology, College of Medicine, Ewha Womans University, Korea.

Copyright ⓒ 1979. Ewha Womans University School of Medicine. This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Published Online: Jul 24, 2015


The urinary bladder consists of two functionally different units, the detrusor and the trigone, and receives autonomic innervations. The beta-adrenergic receptors are responsible for relaxation and prevail in the detrusor, while the alpha-adrenergic ones are responsible for contraction and are present predominantly in the trigone. The parasympathetic innervations are responsible for contraction in the entire urinary bladder muscle. The motor innervation of the urinary bladder is usually represented as cholinergic, therefore contraction of the urinary bladder by muscarinic agents or anticholinesterase is easily blocked by atropine. However, contraction of the urinary bladder by parasympathetic nerve stimulation or ganglionic nicotinic agents is highily resistant to blockade by atropine. Concerning these atropine-resistance phenomena, a number of hypotheses have been advanced to rationalize them. These hypotheses are of two types: 1) the postulate that all postganglionic motor transmission in the urinary bladder is cholinergic and atropine-resistance is due to peculiarities of the tissue or of atropine, and 2) the postulate that at least part of the transmission is noncholinergic. Ambache and Zar (1970) tried an experiment on transmission actions of catecholamine, serotonin, histamine, prostaglandin, and adenosine triphosphate(ATP) in noncholinergic transmission of the urinary bladder, however, they insisted that these substances are not true transmitter released from noncholinergic fibers to the bladder. Recently, evidence has been indicated that a purine nucleotide, probably, ATP, is the transmitter released from nonadrenergic, noncholinergic, inhibitory nerves to the gastrointestinal tract or excitatory nerves to the urinary bladder. It has been shown that purine nucleoddes cause contraction of dog, cat, rat, and rabbit urinary bladder. In this study, using the bladder strips of rabbit, cat, dog, and guinea pig, responses of the urinary bladder to purine nucleotides were observed. In addition, the influence of various blocking agents on the responses of the strip to purine nucleotide was investigated. Bladder strips about 1.5cm in length were carefully isolated from dome and trigone of the rabbit, cat, dog, and guinea pig. They were suspended in a muscle chamber containing 100ml of Tyrode solution maintained at a constant temperature of 38℃. The chamber was aerated with 95% oxygen and 5% carbondioxide bubbling through the bathing fluid by means of sintered glass plate at the bottom. The bladder strip was attached to the Grass force displacement transducer and the motility was recorded on a Grass polygraph(Model 7). When a stable motility level of the strip had been reached, several drugs were added to the muscle chamber and the changes of motility of the strip were observed. The results obtained are as follows; 1. ATP or ADP enhanced the spontaneous contraction of detrusor strip of rabbit, cat, dog, and guinea pig, while it unaffected the motility of trigone strip. 2. Contractile response of detrusor strip to ATP or ADP was not blocked by pretreatment with atropine, phenoxybenzamine, propranolol, procaine, procainamide, lidocaine, oxytocin, or prostaglandin F. 3. Contractile response of detrusor strip to ATP or ADP was blocked by pretreatment with quinidine or quinine. From the above results, it is suggested that the detrusor of urinary bladder is innervated by noncholinergic excitatory purinergic receptor which is blocked by quinidine.