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

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

Author Silva, Valdo Jose Dias da Google Scholar
Gnecchi-Ruscone, Tomaso Google Scholar
Bellina, Valentina Google Scholar
Oliveira, Mauro Google Scholar
Maciel, Leonardo Google Scholar
Campos de Carvalho, Antonio Carlos Google Scholar
Salgado, Helio Cesar Google Scholar
Bergamaschi, Cassia M. Autor UNIFESP Google Scholar
Tobaldini, Eleonora Google Scholar
Porta, Alberto Google Scholar
Montano, Nicola Google Scholar
Institution Univ Milan
Triangulo Mineiro Fed Univ
SL Mandic Hosp
Universidade de São Paulo (USP)
Universidade Federal do Rio de Janeiro (UFRJ)
Universidade Federal de São Paulo (UNIFESP)
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.
Language English
Sponsor Ministero dell' Istruzione, Universita' e della Ricerca Scientifica
Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
Grant number CNPq: 308016/20092
Date 2012-06-01
Published in Experimental Physiology. Hoboken: Wiley-Blackwell, v. 97, n. 6, p. 719-729, 2012.
ISSN 0958-0670 (Sherpa/Romeo, impact factor)
Publisher Wiley-Blackwell
Extent 719-729
Origin http://dx.doi.org/10.1113/expphysiol.2011.063925
Access rights Open access Open Access
Type Article
Web of Science ID WOS:000305460000005
URI http://repositorio.unifesp.br/handle/11600/34917

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