Autonomic cardiovascular regulation in methyl‐CpG‐binding protein 2 (Mecp2) deficient mice

Abstract

The transcription regulating protein Mecp2, which is involved in gene silencing, is deficient in Rett syndrome. There are suggestions that the autonomic nervous system is affected in this X-linked neurodevelopmental disorder. Blood pressure waveforms were sampled by telemetry in mice at 6–8 months. Heart rate variability (HRV) was evaluated from the standard deviation of pulse interval (PI), the range that encompassed 90% of PI and the low frequency to high frequency ratio from spectral analysis of PI in the frequency domain. Atropine produced a greater increase in heart rate in Mecp2+/− (576±22 to 674±10 bpm; ± SEM) compared to wild type (WT) (631±22 to 673±13) (P = 0.038) Vagal blockade resulted in ~ 50% decrease in indices of HRV in both strains. Heart rate decreased in WT from 596±24 to 506±13 following propranolol, which was not different from Mecp2+/−(620±22 to 504±25). There were no significant changes in mean arterial pressure (MAP) after propranolol. HRV changes were the same in both strains Elevating ambient temperature to 32° C resulted in a fall in heart rate (609±25 to 488±46) and MAP (105±3 to 91±3 mmHg) in WT that was not different from Mecp2+/−(617±30 to 473±22) (119±3 to 99±6). The indices for HRV were increased (~35%) in both strains with increased ambient temperature. The autonomic control of cardiovascular regulation in this mouse model of Rett syndrome is similar to wild type. (Supported by HD044453 from NIH)