Nitric oxide-dependent guanylyl cyclase participates in the glutamatergic neurotransmission within the rostral ventrolateral medulla of awake rats

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dc.contributor.authorPinge, Marli Cardoso Martins [UNIFESP]
dc.contributor.authorAraujo, G. C.
dc.contributor.authorLopes, Oswaldo Ubriaco [UNIFESP]
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.date.accessioned2018-06-15T17:38:26Z
dc.date.available2018-06-15T17:38:26Z
dc.date.issued1999-10-01
dc.description.abstractA well-known action of nitric oxide (NO) is to stimulate the soluble form of guanylyl cyclase, evoking an accumulation of cyclic GMP in target cells. The aim of the present study was to examine the effects of inhibition of guanylyl cyclase dependent on NO during cardiovascular responses induced by L-glutamate and S-nitrosoglutathione (SNOG) microinjected into the rostral ventrolateral medulla (RVLM) of awake rats. Three days before the experiments, adult male Wistar rats (280 to 320 g) were anesthetized for implantation of guide cannulas to the desired stereotaxic position (AP=-2.5 mm, L=1.8 mm) in relation to lambda. The cannulas were fixed to the skull with acrylic cement. Twenty-four hours before the experiments, a femoral artery and vein were cannulated for recording arterial pressure (AP) and heart rate (HR) and injection of anesthetic. Unilateral microinjections (100 nL) of L-glutamate (5 nmol/L) and SNOG (2.5 nmol/L) were made into the histologically confirmed RVLM. The cardiovascular responses to these drugs were evaluated before and after microinjection (3 nmol/L, 200 nL) of either methylene blue or oxodiazoloquinoxaline (ODQ). The hypertensive effect of L-glutamate was attenuated by 74% after methylene blue (Delta A=49+/-8 to 13+/-4 mm Hg) and by 80.5% after ODQ (Delta AP=30+/-2 to 6+/-2 mm HS) The increase in AP produced by SNOG was fully blocked by ODQ (Delta AP=39+/-8 to 1+/-2 mm Hg). These data indicate that cyclic GMP mechanisms have a key role in glutamatergic neurotransmission in the RVLM of awake rats, and it is most probable that NO participates: in this response.en
dc.description.affiliationUniv Fed Sao Paulo, Escola Paulista Med, Dept Fisiol, BR-04023060 Sao Paulo, Brazil
dc.description.affiliationUnifespUniv Fed Sao Paulo, Escola Paulista Med, Dept Fisiol, BR-04023060 Sao Paulo, Brazil
dc.description.sourceWeb of Science
dc.format.extent748-751
dc.identifierhttps://doi.org/10.1161/01.HYP.34.4.748
dc.identifier.citationHypertension. Philadelphia: Lippincott Williams & Wilkins, v. 34, n. 4, p. 748-751, 1999.
dc.identifier.doi10.1161/01.HYP.34.4.748
dc.identifier.issn0194-911X
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/43884
dc.identifier.wosWOS:000083486500008
dc.language.isoeng
dc.publisherLippincott Williams & Wilkins
dc.relation.ispartofHypertension
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectglutamic aciden
dc.subjectblood pressure, arterialen
dc.subjectbrainen
dc.subjectnitric oxideen
dc.subjectrostral ventrolateral medullaen
dc.subjectguanylate cyclaseen
dc.titleNitric oxide-dependent guanylyl cyclase participates in the glutamatergic neurotransmission within the rostral ventrolateral medulla of awake ratsen
dc.typeinfo:eu-repo/semantics/article
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