PROSTAGLANDIN E(2)-INDUCED BLADDER HYPERACTIVITY IN NORMAL, CONSCIOUS RATS - INVOLVEMENT OF TACHYKININS
PROSTAGLANDIN E(2)-INDUCED BLADDER HYPERACTIVITY IN NORMAL, CONSCIOUS RATS - INVOLVEMENT OF TACHYKININS
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DOI：
10.1016/s0022-5347(01)67397-x
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发表时间：
1995-06-01
影响因子：
6.6
通讯作者：
ANDERSSON, KE
中科院分区：
文献类型：
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作者：
ISHIZUKA, O;MATTIASSON, A;ANDERSSON, KE
在正常清醒大鼠中，通过连续膀胱测压法研究，膀胱内滴注加兰地尔（PG）E（2）可促进排尿并增加基础膀胱内压。动脉内给予NK 1受体选择性拮抗剂RP 67，580和NK 2受体选择性拮抗剂SR 48，968均减弱该作用，表明该作用是通过刺激NK 1和NK 2受体介导的。动脉内给予PGE（2）在开始排尿反射之前产生膀胱压力的明显增加，表明PG对逼尿肌平滑肌有直接的收缩作用。动脉内PGE（2）的作用不能被动脉内RP 67，580或SR 48，968阻断，这开启了动脉内PGE（2）引起的排尿反射由PG膀胱内给药时引发的反射以外的途径介导的可能性。因此，目前的结果表明，在膀胱附近动脉内给予PGE（2），可能主要通过直接收缩逼尿肌平滑肌来启动正常大鼠的排尿。然而，当膀胱内给药时，PGE（2）可通过从尿道内和/或尿道下神经释放速激肽刺激排尿。这些速激肽又通过刺激NK 1和NK 2受体启动排尿反射。前列腺素类可能通过释放速激肽，导致下尿路炎症性疾病中出现的冲动和膀胱功能亢进。
In normal conscious rats investigated by continuous cystometry, intravesically instilled prostaglandilm (PG) E(2) facilitated micturition and increased basal intravesical pressure. The effect was attenuated by both the NK1 receptor selective antagonist RP 67,580 and the NK2 receptor selective antagonist SR 48,968, given intra-arterially, suggesting that it was mediated by stimulation of both NK1 and NK2 receptors. Intra-arterially given PGE(2) produced a distinct increase in bladder pressure before initiating a micturition reflex, indicating that the PG had a direct contractant effect on the detrusor smooth muscle. The effect of intra-arterial PGE(2) could not be blocked by intra-arterial RP 67,580 or SR 48,968, which opens the possibility that the micturition reflex elicited by intra-arterial PGE(2) was mediated by pathways other than the reflex initiated when the PG was given intravesically. The present results thus suggest that intra-arterial PGE(2), given near the bladder, may initiate micturition in the normal rat chiefly by directly contracting the smooth muscle of the detrusor. However, when given intravesically, PGE(2) may stimulate micturition by releasing tachykinins from nerves in and/or immediately below the urothelium. These tachykinins, in turn, initiate a micturition reflex by stimulating NK1 and NK2 receptors. Prostanoids may, via release of tachykinins, contribute to both urge and bladder hyperactivity seen in inflammatory conditions of the lower urinary tract.