Acute adenosine increases cardiac vagal and reduces sympathetic efferent nerve activities in rats

Show simple item record Silva, Valdo Jose Dias da Gnecchi-Ruscone, Tomaso Bellina, Valentina Oliveira, Mauro Maciel, Leonardo Campos de Carvalho, Antonio Carlos Salgado, Helio Cesar Bergamaschi, Cassia M. [UNIFESP] Tobaldini, Eleonora Porta, Alberto Montano, Nicola 2016-01-24T14:27:16Z 2016-01-24T14:27:16Z 2012-06-01
dc.identifier.citation Experimental Physiology. Hoboken: Wiley-Blackwell, v. 97, n. 6, p. 719-729, 2012.
dc.identifier.issn 0958-0670
dc.description.abstract Adenosine is the first drug of choice in the treatment of supraventricular arrhythmias. While the effects of adenosine on sympathetic nerve activity (SNA) have been investigated, no information is available on the effects on cardiac vagal nerve activity (VNA). We assessed in rats the responses of cardiac VNA, SNA and cardiovascular variables to intravenous bolus administration of adenosine. in 34 urethane-anaesthetized rats, cardiac VNA or cervical preganglionic sympathetic fibres were recorded together with ECG, arterial pressure and ventilation, before and after administration of three doses of adenosine (100, 500 and 1000 mu g kg-1). the effects of adenosine were also assessed in isolated perfused hearts (n= 5). Adenosine induced marked bradycardia and hypotension, associated with a significant dose-dependent increase in VNA (+204 +/- 56%, P < 0.01; +275 +/- 120%, P < 0.01; and +372 +/- 78%, P < 0.01, for the three doses, respectively; n= 7). Muscarinic blockade by atropine (5 mg kg-1, i.v.) significantly blunted the adenosine-induced bradycardia (-56.0 +/- 4.5%, P < 0.05; -86.2 +/- 10.5%, P < 0.01; and -34.3 +/- 9.7%, P < 0.01, respectively). Likewise, adenosine-induced bradycardia was markedly less in isolated heart preparations. Previous barodenervation did not modify the effects of adenosine on VNA. On the SNA side, adenosine administration was associated with a dose-dependent biphasic response, including overactivation in the first few seconds followed by a later profound SNA reduction. Earliest sympathetic activation was abolished by barodenervation, while subsequent sympathetic withdrawal was affected neither by baro- nor by chemodenervation. This is the first demonstration that acute adenosine is able to activate cardiac VNA, possibly through a central action. This increase in vagal outflow could make an important contribution to the antiarrhythmic action of this substance. en
dc.description.sponsorship Ministero dell' Istruzione, Universita' e della Ricerca Scientifica
dc.description.sponsorship Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.format.extent 719-729
dc.language.iso eng
dc.publisher Wiley-Blackwell
dc.relation.ispartof Experimental Physiology
dc.rights Acesso aberto
dc.title Acute adenosine increases cardiac vagal and reduces sympathetic efferent nerve activities in rats en
dc.type Artigo
dc.contributor.institution Univ Milan
dc.contributor.institution Triangulo Mineiro Fed Univ
dc.contributor.institution SL Mandic Hosp
dc.contributor.institution Universidade de São Paulo (USP)
dc.contributor.institution Universidade Federal do Rio de Janeiro (UFRJ)
dc.contributor.institution Universidade Federal de São Paulo (UNIFESP)
dc.description.affiliation Univ Milan, Dept Clin Sci, L Sacco Hosp, I-20157 Milan, Italy
dc.description.affiliation Triangulo Mineiro Fed Univ, Dept Biol Sci, Uberaba, MG, Brazil
dc.description.affiliation SL Mandic Hosp, Div Cardiol, Merate, LC, Italy
dc.description.affiliation Univ São Paulo, Sch Med Ribeirao Preto, Dept Physiol, Ribeirao Preto, SP, Brazil
dc.description.affiliation Univ Fed Rio de Janeiro, Inst Biophys Carlos Chagas Filho, Rio de Janeiro, RJ, Brazil
dc.description.affiliation Universidade Federal de São Paulo, Dept Physiol, São Paulo, Brazil
dc.description.affiliation Univ Milan, Dept Hlth Technol, Galeazzi Orthoped Inst, I-20157 Milan, Italy
dc.description.affiliationUnifesp Universidade Federal de São Paulo, Dept Physiol, São Paulo, Brazil
dc.description.sponsorshipID CNPq: 308016/20092
dc.identifier.doi 10.1113/expphysiol.2011.063925
dc.description.source Web of Science
dc.identifier.wos WOS:000305460000005


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