CENTRAL VAGOTONIC EFFECTS OF ATROPINE MODULATE SPECTRAL OSCILLATIONS OF SYMPATHETIC-NERVE ACTIVITY

Background-Low-dose atropine causes bradycardia either by acting on th e sinoatrial node or by its effects on central muscarinic receptors in creasing vagal activity. Any central muscarinic effects of high-dose a tropine on RR interval are masked by peripheral muscarinic blockade at the sinoatrial node, which causes tachycardia. Effects of central par asympathetic activation on sympathetic activity are not known. Methods and Results-Using power spectral analysis of RR interval, intra-arter ial blood pressure, respiration, and muscle sympathetic nerve activity (MSNA), we examined the effects of bath low (2 mu g/kg IV) and high ( 15 mu g/kg IV) doses of atropine. After low-dose atropine, RR increase d by 9+/-1% (P<0.0001), the low-frequency (LF) component tin normalize d units, NU) of RR variability decreased by -32+/-8%, and the high-fre quency (HF)(NU) component increased (+74+/-19%); hence, LF/KF of RR va riability fell by 52+/-10% (all P<0.01). Although overall MSNA did not change, LFNU of MSNA decreased (-15+/-5%), HFNU of MSNA increased (+3 1+/-3%), and LF/HF of MSNA fell (-41+/-8%) tall P<0.01). After high-do se atropine, LFNU of MSNA decreased (-17+/-12%), HFNU of MSNA increase d (+/-22+/-3%), and LF/HF of MSNA fell (-51+/-21%) (all P<0.02). Concl usions-Increasing central parasympathetic activity with low-dose atrop ine is associated with an increase in the HF and a decrease in the LF oscillations of both RR interval and MSNA variability. High-dose atrop ine similarly induces an increase in the HF and a decrease in the LF c omponents of MSNA variability. Thus, central parasympathetic activatio n is able to modulate the oscillatory characteristics of sympathetic n erve traffic to peripheral blood vessels.