BACKGROUND: The arterial baroreflex is a key mechanism for maintaining blood pressure homeostasis. Low-dose atropine (LDA) causes bradycardia, either by acting on the sinoatrial node or due to its effect on central muscarinic receptors, which increases vagal activity. We evaluated the effect of LDA on baroreflex sensitivity (BRS) in healthy awake subjects.

METHODS: We assessed changes in RR interval (RRI) and systolic blood pressure (SBP), power spectral densities of heart rate variability (HRV) and systolic blood pressure variability (SBPV), and spontaneous BRS by using transfer function analysis before and after LDA (2µg/kg) in 17 healthy volunteers.

RESULTS: LDA induced not only bradycardia but also increased of the high-frequency (HF) component of HRV, RMSSD (root mean squared successive difference interval), and pNN50 (percentage of sinus cycles differing from the preceding cycle by > 50 ms). The HF and LF components of SBPV remained unchanged. Spontaneous BRS determined by transfer function analysis increased significantly (P < 0.05), and changes in BRS were significantly associated with changes in the HF component of HRV (P < 0.05).

CONCLUSIONS: LDA increased vagal cardiac function and arterial baroreflex in awake subjects. This result suggests that increased vagal cardiac function by LDA application is related to baroreflex increase.