Brain nitric oxide induces facilitation of the micturition reflex through brain glutamatergic receptors in rats
Brain nitric oxide induces facilitation of the micturition reflex through brain glutamatergic receptors in rats
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脑一氧化氮通过脑谷氨酸受体诱导大鼠排尿反射的促进
DOI：
10.1002/nau.24440
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发表时间：
2020
影响因子：
2
通讯作者：
Saito Motoaki
中科院分区：
文献类型：
--
作者：
Ono Hideaki;Shimizu Takahiro;Zou Suo;Yamamoto Masaki;Shimizu Yohei;Aratake Takaaki;Hamada Tomoya;Nagao Yoshiki;Shimizu Shogo;Higashi Youichirou;Saito Motoaki
脑内一氧化氮(NO)参与交感神经-肾上腺髓质系统的调节，可影响排尿和储存功能。因此，我们研究了侧脑室注射3-(4-吗啉基)辛尼明盐酸盐(SIN-1)(NO供体)对大鼠排尿反射的影响，重点观察了SIN-1对交感-肾上腺髓质系统的依赖性，以及乌拉坦麻醉(0.8αg/kg，ip)大鼠血浆去甲肾上腺素和肾上腺素的变化以及对脑内N-甲基-D-天冬氨酸和 -氨基-3-羟基-5-甲基-4-异恶唑丙酸受体的影响。结果SIN-1(100和250 微克/只)可升高血浆肾上腺素，缩短收缩间期(110.5%[SIN-1，0 微克]和54.9%[SIN-1,250 微克])，但对血浆去甲肾上腺素和最大排尿压无影响[P<；η<0.05； =0.59]。SIN-1(250 微克/只)减少了单次排尿量和膀胱容量，而不影响排尿后的残余容量。2‐(4‐carboxyphenyl)‐4，4，5，5‐tetramethylimidazoline‐1‐oxyl‐3‐oxide，钠盐(无清除剂，icv)可减弱SIN-1(250 /只)引起的肾上腺素升高和ICI值的降低(ICI值分别为44.7%[Vehicle + SIN-1]和77.5%[Carxy-PTIO + SIN-1])，在SIN-1给药后15 分钟[P<； .05；η2= 0.51]。急性双侧肾上腺切除可阻断SIN-1诱导的肾上腺素升高，但对SIN-1诱导的ICI降低无影响。在SIN-1给药后15 分钟内，MK-801(NMDA受体拮抗剂，icv)可减弱ICI值(47.0%[Vehicle + SIN-1]和87.6%[MK-801 + SIN-1])，但不能被DNQX( 受体拮抗剂，icv)所减弱。结论脑内NO参与易化大鼠排尿反射，而不依赖交感-肾上腺髓质流出调节。
AimBrain nitric oxide (NO) have been reported in regulation of the sympatho‐adrenomedullary system, which can affect voiding and storage functions. Therefore, we investigated effects of intracerebroventricularly (icv) administered 3‐(4‐morpholinyl)sydnonimine, hydrochloride (SIN‐1) (NO donor) on the micturition reflex, focusing on their dependence on the sympatho‐adrenomedullary system and on brainN‐methyl‐D‐aspartate (NMDA) andα‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazole propionate (AMPA) receptors in urethane‐anesthetized (0.8 g/kg, ip) male Wistar rats.MethodsPlasma noradrenaline and adrenaline were measured just before and 5 minutes after SIN‐1 administration. Evaluation of urodynamic parameters was started 1 hour before SIN‐1 administration or intracerebroventricular pretreatment with other drugs.ResultsSIN‐1 (100 and 250 µg/animal) elevated plasma adrenaline and reduced intercontraction interval ([ICI] values; 110.5% [SIN‐1, 0 µg] and 54.9% [SIN‐1, 250 µg] during 15 minutes after SIN‐1 administration [P< .05;η2= 0.59]) without affecting plasma noradrenaline or maximal voiding pressure. SIN‐1 (250 µg/animal) reduced single‐voided volume and bladder capacity without affecting post‐voiding residual volume. The SIN‐1 (250 µg/animal)‐induced adrenaline elevation and ICI reduction were attenuated by 2‐(4‐carboxyphenyl)‐4,4,5,5‐tetramethylimidazoline‐1‐oxyl‐3‐oxide, sodium salt (carboxy‐PTIO) (NO scavenger, icv) (ICI values; 44.7% [vehicle + SIN‐1] and 77.5% [carboxy‐PTIO + SIN‐1] during 15 minutes after SIN‐1 administration [P< .05;η2= 0.51]). Acute bilateral adrenalectomy abolished SIN‐1‐induced adrenaline elevation, while showed no effect on the SIN‐1‐induced ICI reduction. The ICI reduction was attenuated by MK‐801 (NMDA receptor antagonist, icv) (ICI values; 47.0% [vehicle + SIN‐1] and 87.6% [MK‐801 + SIN‐1] during 15 minutes after SIN‐1 administration [P< .05;η2= 0.61]), but not by DNQX (AMPA receptor antagonist, icv).ConclusionBrain NO is involved in facilitation of the rat micturition reflex through brain NMDA receptors, independently of the sympatho‐adrenomedullary outflow modulation.
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影响因子：
5.3
作者：
Lee, S;Kim, CK;Rivier, C
通讯作者：
Rivier, C
影响因子：
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作者：
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影响因子：
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作者：
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通讯作者：
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影响因子：
3.4
作者：
Kelsey Andersson;K. Persson
通讯作者：
K. Persson
影响因子：
3.7
作者：
Neitz, Angela;Mergia, Evanthia;Mittmann, Thomas
通讯作者：
Mittmann, Thomas