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Inhibition of neuronal nitric oxide reduces heart rate variability in the anaesthetised dog

Published online by Cambridge University Press:  24 September 2001

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 AB 25 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 AB 25 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 AB 25 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 AB 25 2ZD, UK
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Abstract

In the vagally intact anaesthetised dog, we have investigated the role of nitric oxide (NO) on a normal sinus arrhythmia using an inhibitor of neuronally released NO, 1-(2-trifluoromethylphenyl) imidazole (TRIM). The mean and S.D. of the R-R interval was used to describe mean heart rate and heart rate variability, respectively. TRIM (0.8 mg I.C.) injected into the sinus node artery increased the mean heart rate slightly but reduced heart rate variability 3-fold from a control of 790 ± 124 ms (mean ± S.D.; n = 5) to 666 ± 36 ms (P < 0.01 Student's paired t test, n = 5). These results suggest that neuronally released NO may have a vagal facilitatory role in the maintenance of sinus arrhythmia in the normal heart. Experimental Physiology (2001) 86.5, 539-541.

Type
Rapid Communications
Information
Experimental Physiology , Volume 86 , Issue 5 , September 2001 , pp. 539 - 541
Copyright
© The Physiological Society 2001

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