An investigation into the physiological relevance of the vagal tachycardia in the anaesthetized dog

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Abstract
Aim:  Our aim was primarily to assess whether or not a vagal tachycardia can be elicited in vivo without administration of atropine, and secondly to evaluate whether the dose of atropine, a muscarinic antagonist, determines the magnitude of the tachycardia.Methods:  Experiments were carried out in the presence of atenolol (2 mg kg−1). The vagal tachycardia requires high vagal activity which was induced by noradrenaline infusion (20 μg min−1). Two techniques were then used to elicit a tachycardia, vagal section and atropine administration.Results:  The increase in blood pressure caused heart rate to fall to 60 ± 7 beats min−1 (mean ± SEM). When the vagi were sectioned (n = 5) heart rate increased by 9 ± 2 beats min−1 above the intrinsic rate which was 108 beats min−1, this increase was not significant. In contrast atropine given (9–20 μg kg−1) (n = 5) during high vagal activity increased heart rate by 81 ± 22 beats min−1 above the intrinsic rate (P < 0.05). To assess if the dose of atropine affects the magnitude of the vagal tachycardia, the right vagus was stimulated electrically at increasing frequencies (2, 4, 8, 16, 32 Hz) before and after increasing doses of atropine (0.02, 0.05, 1 mg kg−1). This reduced the magnitude of the bradycardia; however, the magnitude of the vagal tachycardia was unaffected.Conclusion:  The vagal tachycardia cannot be elicited without atropine suggesting that it does not play a significant physiological role.