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Title: Acute adenosine increases cardiac vagal and reduces sympathetic efferent nerve activities in rats
Authors: 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
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)
Issue Date: 1-Jun-2012
Publisher: Wiley-Blackwell
Citation: Experimental Physiology. Hoboken: Wiley-Blackwell, v. 97, n. 6, p. 719-729, 2012.
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.
ISSN: 0958-0670
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