방광근절편 운동에 미치는 purine nucleotides의 영향

Abstract

[영문]

[한글]

방광은 기능이 서로 다른 배뇨근과 삼각근으로 구성되고 자율신경계의 지배를 받는다.

교감신경 전파물질은 배뇨근의 β-수용체에 작용하여 이완반응을, 삼각근의 α-수용체에

작용하여 수축반응을 일으키며 부교감신경 전파물질은 전 방광근에 작용하여 수축반응을

일으키는 것으로 알려져 있다.

방광의 배뇨활동은 주로 부교감신경인 골반신경을 통하여 이루어진다고 한다. 따라서 m

uscarine성 약물 혹은 anticholinesterase에 의한 방광수축반응은 atropine으로 쉽게 봉

쇄되지만 골반신경자극이나 신경절 흥분제인 nicotine 성 약물에 의할 방광수축반응은 at

ropine으로 쉽게 봉쇄되지 않는다.

이러한 방광기 atropine-resistance현상은 방광근에 분포된 모든 부교감신경절후 섬유

는 cholinergic이지만 근조직 또는 atropine의 특이성 때문에 초래될 것이라는 설 및 부

교감신경 절후 섬유의 일부가 noncholinergic섬유로 되어 있기 때문이라 설명되고 있다.

이런 noncholinergic섬유의 신경전달물질은 acetylcholine이 아닌 다른 인자라고 추측되

고 있다.

최근 위장계, 방광, 혈관계 및 폐등에 nonadrenergic, noncholinergic 신경섬유가 존재

하며 이 섬유의 전달물질은 purine nucleotide인 ATP라고 시사하고 ATP에 대한 평활근의

촉진 또는 억제반응에 관여하는 2개의 수용체가 있을 것이라는 보고가 있다.

이에 본 실험은 purine nucleotides에 대한 수종 동물의 척출방광(剔出膀胱)의 반응을

검토하였고 아울러 이 반응에 대한 각종 차단제의 영향을 검색하여 다음과 같은 결과를

얻었다.

1. ATP 혹은 ADP는 토끼, 고양이, 개 및 해명의 배뇨근절편을 수축시키나 삼자근절편에

는 영향을 주지 않았다

2. ATP 혹은 ADP의 토끼 배뇨근절편 수축작용은 atropine, phenoxyben-zamine. propran

olol, procaine, procainamide, lidocaine, oxytocin 및 prostaglandin F^^2α 전처치로

봉쇄되지 않았다.

3. ATP 혹은 ADP의 토끼 배뇨근절편 수축작용은 quinidine 또는 quinine 전처치로 봉쇄

되었다.

이상의 실험성적으로 방광근 특히 배뇨근에는 quinidine으로 봉쇄되는 non-cholinergic

흥분성 Purinergic receptor가 개재한다고 생각된다.

Effects of Purine Nucleotides on Motility of Urlnary Bladder

Ho Sun Lee

Department of Medical Science The Graduate School, Yonsei University

(Directed by Professors Chong Soon Wang and Sa Suk Hong)

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 trigons. 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 caterholamine,

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 nucleotides cause contraction of dog, cat,

rat, and rabbit urinary bladder.

In this study, using the bladder strips of rabbit, eat, 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 100 ml of Tyrode solution maintained at a constant temperature

of 38℃. The chamber was aerated with 95% oxygen and 5% carbondioxide bubbling

through the bashing 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 contraftion 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^^2α

3. Contractile response of detrusor strip to ATP or ADP was blocked by

pretreatment with quinidine of quinine. From the above results, it is suggested

that the detrusor of urinary bladder is innervated by noncholinergic excitatory

purinereic receptor which is blocked by quinidine.