Accelerated Heart Rate in Pregnant Mice is not Attributable to Responses to Sympathetic Stimulation

Abstract

Pregnancy is associated with an increase in heart rate (HR) which is a risk factor for the development of cardiac arrhythmias. It is unclear whether pregnancy related alterations in heart rate are mediated by changes in cardiac autonomic stimulation and/or alterations in the cardiac conduction system. Therefore the objective of this study was to compare heart rate between pregnant (P) and non-pregnant (NP) mice and determine whether heart rate is influenced by the autonomic nervous system. Initially, surface ECG were recorded from anaesthetized NP, P and post-partum (PP) mice under control conditions. The heart rate was significantly increased in P compared to NP and PP mice (P: 530.8±14.0 bpm, n=15; NP: 469.6±26.5 bpm, n=10; PP: 476.8±16.3 bpm, n=6; p<0.05 P vs NP and PP). Moreover, the response to isoproterenol and propranolol was not significantly different between P and NP mice. In fact, in presence of isoproterenol (100 nM), heart rate increased by 15±4% (n=7) and 27±7% (n=7) in P and NP mice, respectively (p=NS). Whereas, propranolol (250 μM) reduced heart rate by 22±2% (n=7) and 30±4% (n=7) in P and NP mice, respectively (p=NS). This suggests that sympathetic stimulation is not responsible for the increased heart rate observed in pregnant mice. Furthermore, in Langendorff-perfused hearts, heart rate was faster in P compared to NP mice (HR: P 385.83±18.11 bpm, n=11; NP 327.3±15.75 bpm, n=10). Taken together, these results suggest that changes in heart rate in P mice are not attributable to pregnancy-related alterations in the sympathetic innervation of the heart. Thus, it is possible that changes in heart rate in pregnant mice may be mediated by alterations in the cardiac conduction system.