Central Vagotonic Effects of Atropine Modulate Spectral Oscillations of Sympathetic Nerve Activity

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Abstract
Background —Low-dose atropine causes bradycardia either by acting on the sinoatrial node or by its effects on central muscarinic receptors increasing vagal activity. Any central muscarinic effects of high-dose atropine on RR interval are masked by peripheral muscarinic blockade at the sinoatrial node, which causes tachycardia. Effects of central parasympathetic activation on sympathetic activity are not known. Methods and Results —Using power spectral analysis of RR interval, intra-arterial blood pressure, respiration, and muscle sympathetic nerve activity (MSNA), we examined the effects of both low (2 μg/kg IV) and high (15 μg/kg IV) doses of atropine. After low-dose atropine, RR increased by 9±1% ( P NU component increased (+74±19%); hence, LF/HF of RR variability fell by 52±10% (all P NU of MSNA decreased (−15±5%), HF NU of MSNA increased (+31±3%), and LF/HF of MSNA fell (−41±8%) (all P NU of MSNA decreased (−17±12%), HF NU of MSNA increased (+22±3%), and LF/HF of MSNA fell (−51±21%) (all P Conclusions —Increasing central parasympathetic activity with low-dose atropine is associated with an increase in the HF and a decrease in the LF oscillations of both RR interval and MSNA variability. High-dose atropine similarly induces an increase in the HF and a decrease in the LF components of MSNA variability. Thus, central parasympathetic activation is able to modulate the oscillatory characteristics of sympathetic nerve traffic to peripheral blood vessels.