The urinary bladder consists of two funcionally different units, the detrusor and the trigone, and receives autonomic innervations. The beta-adrenergic receptors ar responsible for relaxation and prevail in the detruson, while the alpha-adrenergic ones are responsible for contraction and are present prodominantly in the rtigone. 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 uriary bladder by muscarinic agents or anticholinesterase is easily blocked by atropine. However, contraction of the urinary bladder by parasympathetic nerve stimulationor ganglionic nicontinic 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 postgnglionic motor transmission in the urinary bladder is cholinergic and atropineresistance 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 actionsof catecholamine, serotonin, histamine, prostaglandin, and adenoine 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, inhibitoty nerves to the gastrointestinal tract or excitatory nerves to the urinary bladder. It has been shown that purine nucleotides cause contraction of dog, cat, rat, and rabbit ruinary bladder.
In this study, using the bladder strips of rabbit, cat, dog, and guinea pig, responses of the urinary ladder to purine nucloeotides were obseved. In addition. the influence of various blocking agents on the responses of the strip to purine nucleotide was investigated.
Bladder strips about 1.5 cm 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 100㎖ of tyrode solution maintained at a constant temperature of 38℃. The chamber was aerated with 95% oxygen and 5% carbondioxide bubbing 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 mucle 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, procainamide, lidocaine, oxytocin, or prostaglandin F_(2α).
3. Contractile responce of detrusor strip to APT 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
|