Miyazato Minoru, Kaiho Yasuhiro, Kamo Izumi, Kitta Takeya, Chancellor Michael B, Sugaya Kimio, Arai Yoichi, de Groat William C, Yoshimura Naoki
Dept. of Urology, Univ. of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA.
Am J Physiol Renal Physiol. 2009 Oct;297(4):F1024-31. doi: 10.1152/ajprenal.00297.2009. Epub 2009 Jul 29.
To clarify the role of spinal serotonergic mechanisms in preventing stress urinary incontinence (SUI) during sneezing, we investigated the effect of intrathecal (it) application of 8-OH-DPAT (a 5-HT(1A) agonist), mCPP (a 5-HT(2B/2C) agonist), and fluoxetine (a serotonin reuptake inhibitor) using a rat model that can examine the neurally evoked continence reflex during sneezing. Amplitudes of urethral pressure responses during sneezing (A-URS), urethral baseline pressure (UBP) at the midurethra, and sneeze-induced leak point pressure (S-LPP) were measured in normal female adult rats and rats with SUI induced by vaginal distention (VD). In normal rats, 8-OH-DPAT decreased A-URS by 48.9%, whereas mCPP increased A-URS by 33.6%. However, A-URS was not changed after fluoxetine. 8-OH-DPAT, mCPP, or fluoxetine did not alter UBP. The effect of 8-OH-DPAT and mCPP was antagonized by WAY-100635 (it), a selective 5-HT(1A) antagonist, and RS-102221 (it), a selective 5-HT(2C) antagonist, respectively. Fluoxetine in the presence of WAY-100635 did not change either A-URS or UBP, but fluoxetine in the presence of RS-102221 decreased A-URS. In VD rats, S-LPP was decreased by 14.6 cmH2O after 8-OH-DPAT, whereas it was increased by 12.8 cmH2O after mCPP. However, S-LPP was not changed after fluoxetine. These results indicate that activation of 5-HT(2C) receptors enhances the active urethral closure reflex during sneezing at the spinal level, whereas 5-HT(1A) inhibits it and that no apparent changes in the sneeze-induced continence reflex after fluoxetine treatment are due to coactivation of excitatory 5-HT(2C) receptors and inhibitory 5-HT receptors other than the 5-HT(1A) subtype. Thus, activation of excitatory 5-HT receptor subtypes such as 5-HT(2C) could be effective for the treatment of SUI.
为阐明脊髓5-羟色胺能机制在打喷嚏时预防压力性尿失禁(SUI)中的作用,我们使用一种能够检测打喷嚏时神经诱发的控尿反射的大鼠模型,研究了鞘内注射8-OH-DPAT(一种5-HT(1A)激动剂)、mCPP(一种5-HT(2B/2C)激动剂)和氟西汀(一种5-羟色胺再摄取抑制剂)的效果。在正常成年雌性大鼠和阴道扩张(VD)诱导的SUI大鼠中,测量了打喷嚏时尿道压力反应的幅度(A-URS)、尿道中段的基线压力(UBP)以及打喷嚏诱发的漏点压力(S-LPP)。在正常大鼠中,8-OH-DPAT使A-URS降低了48.9%,而mCPP使A-URS增加了33.6%。然而,氟西汀处理后A-URS没有变化。8-OH-DPAT、mCPP或氟西汀均未改变UBP。8-OH-DPAT和mCPP的作用分别被选择性5-HT(1A)拮抗剂WAY-100635(鞘内注射)和选择性5-HT(2C)拮抗剂RS-102221(鞘内注射)拮抗。在WAY-100635存在的情况下,氟西汀既不改变A-URS也不改变UBP,但在RS-102221存在的情况下,氟西汀降低了A-URS。在VD大鼠中,8-OH-DPAT使S-LPP降低了14.6 cmH2O,而mCPP使其增加了12.8 cmH2O。然而,氟西汀处理后S-LPP没有变化。这些结果表明,5-HT(2C)受体的激活在脊髓水平增强了打喷嚏时主动尿道关闭反射,而5-HT(1A)抑制该反射,并且氟西汀治疗后打喷嚏诱发的控尿反射无明显变化是由于兴奋性5-HT(2C)受体和除5-HT(1A)亚型以外的抑制性5-HT受体的共同激活。因此,激活兴奋性5-HT受体亚型如5-HT(2C)可能对SUI的治疗有效。