The increase of respiratory sinus arrhythmia during low dose atropine is not due to changes of the sinus node transfer function or baroreflex

Low dose of atropine increases heart period and respiratory sinus arrhythmia, while at high doses the peripheral parasympathetic blockade becomes appreciable. The mechanisms underlying this phenomenon are investigated in a set of 10 healthy young humans by means of a linear causal open loop model. This model allows us to contemporaneously and non invasively derive an estimate of the sinus node transfer function and of the baroreflex gain. Neither the dynamic properties of the sinus node nor the baroreflex gain appear to be modified by the low dose administration of atropine. These results support the conclusion that the increase of respiratory sinus arrhythmia does not depend on either a modification of the transduction properties at the sinus node level or an increased responsiveness of the baroreflex but may have a central origin.