Central nitric oxide modulates hindquarter vasodilation elicited by AMPA receptor stimulation in the NTS of conscious rats

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dc.contributor.authorDias, Ana Carolina Rodrigues
dc.contributor.authorColombari, Eduardo [UNIFESP]
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.contributor.institutionUniv Estadual São Paulo
dc.date.accessioned2016-01-24T12:41:08Z
dc.date.available2016-01-24T12:41:08Z
dc.date.issued2006-05-01
dc.description.abstractMicroinjection of S-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid ( AMPA) in the nucleus of the solitary tract (NTS) of conscious rats causes hypertension, bradycardia, and vasoconstriction in the renal, mesenteric, and hindquarter vascular beds. in the hindquarter, the initial vasoconstriction is followed by vasodilation with AMPA doses > 5 pmol/100 nl. To test the hypothesis that this vasodilation is caused by activation of a nitroxidergic pathway in the NTS, we examined the effect of pretreatment with the nitric oxide synthase inhibitor N-G-nitro-L- arginine methyl ester (L-NAME, 10 nmol/ 100 nl, microinjected into the NTS) on changes in mean arterial pressure, heart rate, and regional vascular conductance (VC) induced by microinjection of AMPA ( 10 pmol/100 nl in the NTS) in conscious rats. AMPA increased hindquarter VC by 18 +/- 4%, but after pretreatment with L-NAME, AMPA reduced hindquarter VC by 16 +/- 7% and 17 +/- 9% ( 5 and 15 min after pretreatment, P < 0.05 compared with before pretreatment). Pretreatment with L-NAME reduced AMPA-induced bradycardia from 122 +/- 40 to 92 +/- 32 beats/min but did not alter the hypertension induced by AMPA ( 35 +/- 5 mmHg before pretreatment, 43 +/- 6 mmHg after pretreatment). Control injections with D-NAME did not affect resting values or the response to AMPA. the present study shows that stimulation of AMPA receptors in the NTS activates both vasodilatatory and vasoconstrictor mechanisms and that the vasodilatatory mechanism depends on production of nitric oxide in the NTS.en
dc.description.affiliationUniversidade Federal de São Paulo, Dept Physiol, EPM, BR-0402360 São Paulo, Brazil
dc.description.affiliationUniv Estadual São Paulo, Dept Pathol & Physiol, Araraquara, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Dept Physiol, EPM, BR-0402360 São Paulo, Brazil
dc.description.sourceWeb of Science
dc.format.extentR1330-R1336
dc.identifierhttp://dx.doi.org/10.1152/ajpregu.00150.2005
dc.identifier.citationAmerican Journal of Physiology-regulatory Integrative and Comparative Physiology. Bethesda: Amer Physiological Soc, v. 290, n. 5, p. R1330-R1336, 2006.
dc.identifier.doi10.1152/ajpregu.00150.2005
dc.identifier.issn0363-6119
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/28863
dc.identifier.wosWOS:000236664400021
dc.language.isoeng
dc.publisherAmer Physiological Soc
dc.relation.ispartofAmerican Journal of Physiology-regulatory Integrative and Comparative Physiology
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectnitric oxide synthaseen
dc.subjectregional vascular conductanceen
dc.subjectcardiovascular regulationen
dc.titleCentral nitric oxide modulates hindquarter vasodilation elicited by AMPA receptor stimulation in the NTS of conscious ratsen
dc.typeinfo:eu-repo/semantics/article
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