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Nitric oxide facilitates vagal control of heart rate via actions in the cardiac parasympathetic ganglia of the anaesthetised dog

Published online by Cambridge University Press:  18 January 2002

F. Markos ,
H. M. Snow ,
C. Kidd  and
K. Conlon
F. Markos
Affiliation:
Department of Physiology, University College Cork, Cork, Ireland and Department of Biomedical Sciences, Medical School, Foresterhill Campus, University of Aberdeen, Aberdeen AB25 2ZD, UK
H. M. Snow
Affiliation:
Department of Physiology, University College Cork, Cork, Ireland and Department of Biomedical Sciences, Medical School, Foresterhill Campus, University of Aberdeen, Aberdeen AB25 2ZD, UK
C. Kidd
Affiliation:
Department of Physiology, University College Cork, Cork, Ireland and Department of Biomedical Sciences, Medical School, Foresterhill Campus, University of Aberdeen, Aberdeen AB25 2ZD, UK
K. Conlon
Affiliation:
Department of Physiology, University College Cork, Cork, Ireland and Department of Biomedical Sciences, Medical School, Foresterhill Campus, University of Aberdeen, Aberdeen AB25 2ZD, UK
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Abstract

The effects of neuronal inhibition of nitric oxide (NO) production on the bradycardia resulting from stimulation of preganglionic and postganglionic parasympathetic fibres were investigated in an anaesthetised dog preparation following transection of the cervical vagi and in the presence of a β-adrenoreceptor antagonist. Injection of 1-(2-trifluoromethylphenyl) imidazole (TRIM), an inhibitor of neuronally released NO, into the sinus node artery reduced the bradycardia evoked by right cervical vagal stimulation. In contrast, when the response to preganglionic stimulation had been abolished by hexamethonium (10 mg kg-1), the bradycardia following stimulation of postganglionic parasympathetic fibres on the atrial epicardium was unaffected by TRIM. First, these results confirm the facilitatory actions of neuronally released NO on vagal heart responses in the dog. Second, they indicate that this modulatory and facilitatory role of NO is likely to be exerted at vagal preganglionic-postganglionic synaptic mechanisms in the cardiac parasympathetic ganglia and not at the postganglionic-sinoatrial node synapse. Experimental Physiology (2002) 87.1, 49-52.

Type
Full Length Papers
Information
Experimental Physiology , Volume 87 , Issue 1 , January 2002 , pp. 49 - 52
Copyright
© The Physiological Society 2002

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