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

Valdo Jose Dias da Silva, Tomaso Gnecchi-Ruscone, Valentina Bellina, Mauro Oliveira, Leonardo Maciel, Antonio Carlos Campos de Carvalho, Helio Cesar Salgado, Cassia M. Bergamaschi, Eleonora Tobaldini, Alberto Porta, Nicola Montano

Research output: Contribution to journalArticlepeer-review


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 μg 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.

Original languageEnglish
Pages (from-to)719-729
Number of pages11
JournalExperimental Physiology
Issue number6
Publication statusPublished - Jun 2012

ASJC Scopus subject areas

  • Physiology


Dive into the research topics of 'Acute adenosine increases cardiac vagal and reduces sympathetic efferent nerve activities in rats'. Together they form a unique fingerprint.

Cite this