Role of pressor mechanisms from the NTS and CVLM in control of arterial pressure

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dc.contributor.authorMoreira, Thiago Santos [UNIFESP]
dc.contributor.authorSato, Monica Akemi
dc.contributor.authorTakakura, Ana Carolina Thomaz [UNIFESP]
dc.contributor.authorMenani, Jose Vanderlei
dc.contributor.authorColombari, Eduardo [UNIFESP]
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.contributor.institutionUNESP
dc.contributor.institutionUniversidade Federal do ABC (UFABC)
dc.date.accessioned2016-01-24T12:38:07Z
dc.date.available2016-01-24T12:38:07Z
dc.date.issued2005-11-01
dc.description.abstractIn the present study, we investigated the effects of inhibition of the caudal ventrolateral medulla (CVLM) with the GABA(A) agonist muscimol combined with the blockade of glutamatergic mechanism in the nucleus of the solitary tract (NTS) with kynurenic acid (kyn) on mean arterial pressure (MAP), heart rate (HR), and regional vascular resistances. in male Holtzman rats anesthetized intravenously with urethane/chloralose, bilateral injections of muscimol (120 pmol) into the CVLM or bilateral injections of kyn (2.7 nmol) into the NTS alone increased MAP to 186 +/- 11 and to 142 +/- 6 mmHg, respectively, vs. control: 105 +/- 4 mmHg; HR to 407 +/- 15 and to 412 +/- 18 beats per minute (bpm), respectively, vs. control: 352 +/- 12 bpm; and renal, mesenteric and hindquarter vascular resistances. However, in rats with the CVLM bilaterally blocked by muscimol, additional injections of kyn into the NTS reduced MAP to 88 +/- 5 mmHg and mesenteric and hindquarter vascular resistances below control baseline levels. Moreover, in rats with the glutamatergic mechanisms of the NTS blocked by bilateral injections of kyn, additional injections of muscimol into the CVLM also reduced MAP to 92 +/- 2 mmHg and mesenteric and hindquarter vascular resistances below control baseline levels. Simultaneous blockade of NTS and CVLM did not modify the increase in HR but also abolished the increase in renal vascular resistance produced by each treatment alone. the results suggest that important pressor mechanisms arise from the NTS and CVLM to control vascular resistance and arterial pressure under the conditions of the present study.en
dc.description.affiliationUniversidade Federal de São Paulo, Dept Physiol, EPM, São Paulo, Brazil
dc.description.affiliationUNESP, Fac Odontol, Dept Physiol & Pathol, Araraquara, Brazil
dc.description.affiliationABC, Fac Med, Dept Physiol, Santo Andre, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Dept Physiol, EPM, São Paulo, Brazil
dc.description.sourceWeb of Science
dc.format.extentR1416-R1425
dc.identifierhttp://dx.doi.org/10.1152/ajpregu.00053.2005
dc.identifier.citationAmerican Journal of Physiology-regulatory Integrative and Comparative Physiology. Bethesda: Amer Physiological Soc, v. 289, n. 5, p. R1416-R1425, 2005.
dc.identifier.doi10.1152/ajpregu.00053.2005
dc.identifier.issn0363-6119
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/28522
dc.identifier.wosWOS:000232528200025
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.subjectventrolateral medullaen
dc.subjectgammaen
dc.subjectgamma-aminobutyric aciden
dc.subjectL-glutamateen
dc.subjectmuscimolen
dc.subjectsympathetic systemen
dc.titleRole of pressor mechanisms from the NTS and CVLM in control of arterial pressureen
dc.typeinfo:eu-repo/semantics/article
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