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Cardiovascular Research 1987 21(10):717-724; doi:10.1093/cvr/21.10.717
© 1987 by European Society of Cardiology
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Copyright © 1987, European Society of Cardiology

Time dependent impairment of vagally mediated inhibition of noradrenaline release in the dog heart

YASUYUKI FURUKAWA*, YASUHIRO OGIWARA*, KIMIAKI SAEGUSA*, MASAYOSHI TAKEDA*, HITOMI TSUBOTA{dagger}, AKIHIRO TADA{dagger}, HIROSHI ZENDA{dagger} and SHIGETOSHI CHIBA*

*From the Department of Pharmacology, Shinshu University School of Medicine, Shinsu University Hospital, Matsumoto, Japan
{dagger}From Department of Pharmacy, Shinsu University Hospital, Matsumoto, Japan

The effects of right vagal nerve stimulation on changes in heart rate, mean coronary sinus blood flow, and noradrenaline overflow rate induced by right cardiac sympathetic nerve stimulation were investigated in anaesthetised decentralised, open chest dogs, when autonomic nerve fibres were stimulated tonically at a frequency of 4 or 5 Hz for 2.5 min. Sympathetic nerve stimulation produced a mean(SEM) increase in each of the variables (50(7.0)% in heart rate, 48(6.3)% in coronary sinus blood flow, and 87.0(12.3) ng·min–1 in noradrenaline overflow rate into coronary sinus blood at 30 s), and the increments remained almost constant during continued stimulation. Vagal nerve stimulation induced a decrease of 34(3.4)% in heart rate and of 22(4.5)% in coronary sinus blood flow and a slight reduction (-9(3.2) ng·min–1) in noradrenaline overflow rate at 30 s. Only the decrease in heart rate faded slightly with time. Combined stimulation of the sympathetic and parasympathetic nerves induced a decrease of 19(5.0)% in heart rate and 4(7.5)% in coronary sinus blood flow and an increase of 34.3(12.0) ng·min–1 in noradrenaline overflow rate at 30 s. The decrease in heart rate and coronary sinus blood flow faded, and noradrenaline overflow rate increased significantly to 86.4(17.3) ng·min–1 at 120 s. The temporal changes in heart rate, coronary sinus blood flow, and noradrenaline overflow rate caused by combined nerve stimulation were readily inhibited by treatment with atropine. These results suggest that (a) temporal suppression of vagal nerve stimulation due to increases in heart rate, coronary sinus blood flow, and noradrenaline overflow rate induced by sympathetic nerve stimulation is mediated through muscarinic receptors and (b) the muscarinic inhibition may occur at prejunctional as well as at postjunctional sites in dog hearts.

KEYWORDS acetylcholine; heart rate; noradrenaline; sympathetic nerves; sympathetic-parasympathetic interaction; vagal nerves

Address for correspondence and reprints: Dr S Chiba, Department of Pharmacology, Shinshu University School of Medicine, Matsumoto 390, Japan.


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