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Therefore, we investigated effects of intracerebroventricularly (icv) administered 3\u2010(4\u2010morpholinyl)sydnonimine, hydrochloride (SIN\u20101) (NO donor) on the micturition reflex, focusing on their dependence on the sympatho\u2010adrenomedullary system and on brain <jats:italic>N<\/jats:italic>\u2010methyl\u2010D\u2010aspartate (NMDA) and <jats:italic>\u03b1<\/jats:italic>\u2010amino\u20103\u2010hydroxy\u20105\u2010methyl\u20104\u2010isoxazole propionate (AMPA) receptors in urethane\u2010anesthetized (0.8\u2009g\/kg, ip) male Wistar rats.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Plasma noradrenaline and adrenaline were measured just before and 5\u2009minutes after SIN\u20101 administration. Evaluation of urodynamic parameters was started 1\u2009hour before SIN\u20101 administration or intracerebroventricular pretreatment with other drugs.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>SIN\u20101 (100 and 250\u2009\u00b5g\/animal) elevated plasma adrenaline and reduced intercontraction interval\u00a0([ICI]\u00a0values; 110.5% [SIN\u20101, 0\u2009\u00b5g]\u00a0and 54.9% [SIN\u20101, 250\u2009\u00b5g]\u00a0during 15\u2009minutes after SIN\u20101 administration [<jats:italic>P<\/jats:italic>\u2009&lt;\u2009.05;\u00a0<jats:italic>\u03b7<\/jats:italic><jats:sup>2<\/jats:sup>\u2009=\u20090.59]) without affecting plasma noradrenaline or maximal voiding pressure. SIN\u20101 (250\u2009\u00b5g\/animal) reduced single\u2010voided volume and bladder capacity without affecting post\u2010voiding residual volume. The SIN\u20101 (250\u2009\u00b5g\/animal)\u2010induced adrenaline elevation and ICI reduction were attenuated by 2\u2010(4\u2010carboxyphenyl)\u20104,4,5,5\u2010tetramethylimidazoline\u20101\u2010oxyl\u20103\u2010oxide, sodium salt (carboxy\u2010PTIO) (NO scavenger, icv) (ICI values; 44.7% [vehicle\u2009+\u2009SIN\u20101]\u00a0and 77.5% [carboxy\u2010PTIO\u2009+\u2009SIN\u20101]\u00a0during 15\u2009minutes after SIN\u20101 administration [<jats:italic>P<\/jats:italic>\u2009&lt;\u2009.05;\u00a0<jats:italic>\u03b7<\/jats:italic><jats:sup>2<\/jats:sup>\u2009=\u20090.51]). Acute bilateral adrenalectomy\u00a0abolished SIN\u20101\u2010induced adrenaline elevation, while showed no effect on the SIN\u20101\u2010induced ICI reduction. The ICI reduction was attenuated by MK\u2010801 (NMDA receptor antagonist, icv) (ICI values; 47.0% [vehicle\u2009+\u2009SIN\u20101]\u00a0and 87.6% [MK\u2010801\u2009+\u2009SIN\u20101]\u00a0during 15\u2009minutes after SIN\u20101 administration [<jats:italic>P<\/jats:italic>\u2009&lt;\u2009.05;\u00a0<jats:italic>\u03b7<\/jats:italic><jats:sup>2<\/jats:sup>\u2009=\u20090.61]), but not by DNQX (AMPA receptor antagonist, icv).<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Brain NO is involved in facilitation of the rat micturition reflex through brain NMDA receptors, independently of the sympatho\u2010adrenomedullary outflow modulation.<\/jats:p><\/jats:sec>","DOI":"10.1002\/nau.24440","type":"journal-article","created":{"date-parts":[[2020,6,19]],"date-time":"2020-06-19T15:59:25Z","timestamp":1592582365000},"page":"1687-1699","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":6,"title":["Brain nitric 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