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dc.contributor.authorDias, ACR
dc.contributor.authorVitela, M.
dc.contributor.authorColombari, Eduardo [UNIFESP]
dc.contributor.authorMifflin, S. W.
dc.identifier.citationAmerican Journal of Physiology-heart and Circulatory Physiology. Bethesda: Amer Physiological Soc, v. 288, n. 1, p. H256-H262, 2005.
dc.description.abstractThe neuromodulatory effect of NO on glutamatergic transmission has been studied in several brain areas. Our previous single-cell studies suggested that NO facilitates glutamatergic transmission in the nucleus of the solitary tract (NTS). in this study, we examined the effect of the nitric oxide synthase (NOS) inhibitor NG-nitro-L-arginine methyl ester (L-NAME) on glutamatergic and reflex transmission in the NTS. We measured mean arterial pressure (MAP), heart rate (HR), and renal sympathetic nerve activity (RSNA) from Inactin-anesthetized Sprague-Dawley rats. Bilateral microinjections of L-NAME (10 nmol/100 nl) into the NTS did not cause significant changes in basal MAP, HR, or RSNA. Unilateral microinjection of (RS)-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA, 1 pmol/100 nl) into the NTS decreased MAP and RSNA. Fifteen minutes after L-NAME microinjections, AMPA-evoked cardiovascular changes were significantly reduced. N-methyl-D-aspartate (NMDA, 0.5 pmol/100 nl) microinjection into the NTS decreased MAP, HR, and RSNA. NMDA-evoked falls in MAP, HR, and RSNA were significantly reduced 30 min after L-NAME. To examine baroreceptor and cardiopulmonary reflex function, L-NAME was microinjected at multiple sites within the rostro-caudal extent of the NTS. Baroreflex function was tested with phenylephrine (PE, 25 mug iv) before and after L-NAME. Five minutes after L-NAME the decrease in RSNA caused by PE was significantly reduced. To examine cardiopulmonary reflex function, phenylbiguanide (PBG, 8 mug/kg) was injected into the right atrium. PBG-evoked hypotension, bradycardia, and RSNA reduction were significantly attenuated 5 min after L-NAME. Our results indicate that inhibition of NOS within the NTS attenuates baro- and cardiopulmonary reflexes, suggesting that NO plays a physiologically significant neuromodulatory role in cardiovascular regulation.en
dc.publisherAmer Physiological Soc
dc.relation.ispartofAmerican Journal of Physiology-heart and Circulatory Physiology
dc.rightsAcesso aberto
dc.subject(RS)-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic aciden
dc.subjectN-methyl-D aspartateen
dc.subjectbaroreceptor and cardiopulmonary reflexesen
dc.subjectcardiovascular regulationen
dc.subjectrenal sympathetic nerve activityen
dc.titleNitric oxide modulation of glutamatergic, baroreflex, and cardiopulmonary transmission in the nucleus of the solitary tracten
dc.contributor.institutionUniv Texas
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.description.affiliationUniv Texas, Hlth Sci Ctr, Dept Pharmacol, San Antonio, TX 78229 USA
dc.description.affiliationUniversidade Federal de São Paulo, Escola Paulista Med, Dept Physiol, São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Escola Paulista Med, Dept Physiol, São Paulo, Brazil
dc.description.sourceWeb of Science

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