요배출시 요도출구의 기능에 영향을 미치는 신경인성 요소에 대한 동물 실험: 요도 확장에 있어 Nitric Oxide 및 베타 교감 신경체의 작용
Neural Factors Controlling Urethral Outlet Activity in vivo: Role of Nitric Oxide and β-Adrenergic System in Urethral Relaxation
전병규, 박흠례,
소속 상세정보
전병규 ( )
고려대학교
박흠례 ( )
고려대학교 의과대학 비뇨기과학교실
KMID : 0358319970380090912
Abstract
결론
Urethane 마취하의 흰쥐를 이용한 방광 및 요도압력측정에서 흰쥐의 방광은 배뇨반사를
유발하는 일정한 방광용적 이상의 요량에 도달하면 반사적 방광수축이 나타나며 이와 동시
에 요도괄약근은 반사적 이완을 하여 조화로운 배뇨과정을 수행하는 것을 확인하였다. 이때
요도의 이완에 관여하는 인자로서 NO경로가 배뇨시 요도평활근의 반사적 이완을 수행하며
베타 교감신경도 NO경로와 함께 요도의 이완반응에 관여함을 알 수 있었다. 알파 교감신경
은 안정시 요도평활근의 긴장을 유지하여 요자제를 유지하며 알파 교감제 투여시 반사적 요
도이완 과정이 차단됨을 알 수 있었다.
#초록#
Aims of Study: During reflex micturition, the urethral outlet remains open (relaxed) to
promote urinary emptying. The mechanisms involved in the relaxation of urethral outlet
is thought to be complex including nitric oxide (NO) pathway and β-adrenergic
activity. The aims of the study focused on these several issues related to the neural
control of urethral outlet in vivo.
Materials & Methods: Female rats weighing 200∼300 gm were anesthetized wish
urethane. Catheters were inserted into femoral artery for drug administration.4 two-way
catheter (16 G angiocath) was inserted into the bladder for saline infusion and pressure
monitoring. A separate cannula (PE 50) was placed into the urethra via external urethral
meatus or proximal urethrat opening to record urethral pressure. The bladder was filled
with saline at a rate of 0.1 ㎖/min to induce reflex micturition. Urethral pressure was
recorded via cannula through which saline was infused at a rate of 0.05 ㎖/min.
Isovolumetric bladder contraction and urethral pressure were recorded simultaneously.
After an equilibration period of 30 minutes, baseline intravesical and urethral pressure
were recorded for 10 minutes prior to drug administration.
NG-nitro-L-arginine methylester (L-NAME, 10 to 15 ㎎/㎏, i.v.),
L-arginine (150 ㎎/㎏, i.v.), propranolol (1 uM., 0.1 ㎖/250 ㎎, i.a.), and phenylephrine (1
0∼100 uM, i.a.) were administrated.
Results: During isovolumetric bladder contraction, urethral pressure was decreased
simultaneously, and then returned to the resting states in conjunction with end of the
bladder contraction. After the administration of L-NAME, the magnitude of reflex
urethral relaxation was decreased significantly (42.6 ± 15.1% of the control, p<0.01),
and this effect was reversed by addition of L-arginine. Administration of propranolol
also inhibited urethral relaxation (66.4% of the control). Administration of L-NAME
followed by propranolol almost completely abolished the urethral relaxation.
Administration of phenylephrine increased the resting urethral tone (mean; 4
cmH2O) significantly, and the magnitude of urethral relaxation was
decreased substantially.
Conclusion: These results suggest that urethral relaxation is mediated by several
neural factors. NO seems like to a potent mediator in a reflex relaxation of the urethral
smooth muscle during micturition. Also, β-adrenergic stimulation play an important role
for urethral relaxation. α-adrenergic nerve discharge, contributed to contraction of
urethral smooth muscle, shows inhibitory effect against the reflex urethral relaxation.
키워드
Urethral relaxation; Nitric oxide; β-adrenergics;
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