Stress cardiovascular/autonomic interactions in mice

Studies evaluated the role of the autonomic nervous system in the cardiovascular response to stress using radiotelemetric blood pressure (BP) recording coupled with autoregressive spectral analysis. Conscious male C57/BL6 mice with carotid arterial telemetric catheters were exposed to acute episodes of shaker stress before and after administration of cholinergic, β 1-adrenergic and α 1-adrenergic receptor antagonists. Pulse interval (PI) and systolic arterial pressure (SAP) were analyzed for variance and the low frequency (LF: 0.1–1.0 Hz) and high frequency (HF: 1–5 Hz) spectral components. Stress (5 min) increased BP and heart rate (HR) as well as PI and SAP variability. PI variance increased from 41 ± 6 to 75 ± 14 ms 2 while SAP variance increased from 25 ± 5 to 55 ± 9 mm Hg 2. Autonomic blockade had specific effects on stress-induced changes in PI and SAP and their respective variability. Atropine reduced the tachycardia and abolished the increase in PI variance and its LF component. Data documents that in mice the cholinergic system is fundamental for the maintenance of HR variability. Atropine had no effects on the BP responses, either the increase in SAP or the variance associated with stress. Atenolol blocked the increase in PI and SAP variability induced by stress. Prazosin reduced the tachycardia produced by stress and blocked the increase in PI (only LF) and SAP variability. Using quantitative spectral analysis of telemetrically collected BP data in mice along with pharmacological antagonism, we were able to accurately determine the role of autonomic input in the mediation of the stress response. Data verify the role of sympathetic/parasympathetic balance in stress-induced changes in HR, BP and indices of variance.