Phenotypic differences in the hemodynamic response during REM sleep in six strains of inbred mice

The pattern of cardiovascular changes that occur at nighttime can have an impact on morbidity and mortality. Rapid-eye-movement (REM) sleep, in particular, represents a period of increased risk due to marked cardiovascular instability. We hypothesized that genetic differences between inbred strains of mice would affect the phenotypic expression of cardiovascular responses that occur in REM sleep. We monitored polysomnography and arterial blood pressure (PSA) simultaneously in six inbred strains of mice as they naturally cycled through sleep/wake states. Two strains elevated their PSA above non-REM (NREM) levels for 57.9 +/- 6.6% (BALB/cJ) and 51.8 +/- 8.4% (DBA/2J) of the REM period and exhibited a significant (P < 0.05) number of PSA surges greater than 10 mmHg (0.78 +/- 0.36 surges/min for BALB/cJ; 0.63 +/- 0.13 surges/min for DBA/2J). Despite similar PSA responses, the DBA/2J strain exhibited a decreased heart rate and the BALB/cJ strain exhibited an increased heart rate during REM sleep. The four other strains (A/J, C57BL/6J, C3H/HeJ, and CBA/J) exhibited a significant hypotensive response associated with no change in heart rate in three of the strains and a significant decrease in heart rate in the A/J strain. The overall variability in PSA during REM sleep was significantly greater in the C3H/HeJ strain (26.8 +/- 2.0 mmHg; P < 0.0125) compared with the other five strains. We conclude that genetic background contributes to the magnitude, variability, and arterial baroreceptor buffering capacity of cardiovascular responses during REM sleep.