In various diseased states reduced cardiac vagal modulation (CVM) is accompanied by impaired endothelial function. It is unclear whether CVM and endothelial function undergo dysregulation independently, or these systems affect each other negatively as a consequence of the disease process. Since the respective physiology is unclear, we aimed to investigate if such relationship between CVM and endothelial function exists in healthy subjects.

46 young males were studied. From 10 minute long ECG recordings mean RR interval (RRI) and time and frequency domain vagal heart rate variability (HRV) indices (SDNN; RMSSD; pNN50 and HF, respectively) were determined. HRV indices were used to define CVM. Endothelial function was assessed by measuring brachial artery flow mediated dilation (FMD). Hyperemic, diastolic shear rate was used to normalize FMD (nFMD).

RRI was related to most HRV indices, but not to FMD. On the other hand, all HRV indices correlated significantly and positively with FMD across subjects (r = 0.49, p<0.01 for HF–nFMD). After adjusting for potential confounders, RMSSD and HF remained significantly associated with nFMD. When subjects were dichotomized according to median RRI, the HRV–nFMD relations lost significance at higher (RRI<910 ms), and gained further significance at lower (RRI>910 ms) heart rates (r = 0.57, p<0.01 for HF–nFMD).

Our data demonstrate that vagal HRV indices are related to FMD across healthy male subjects. Although RRI is not related to FMD, the HRV-FMD relation is dependent upon RRI. The underlying mechanism may involve centrally released endothelial mediators, which enhance CVM through vasculo-neural communication.