The autonomic control of respiratory-related arterial pressure variability (RAPV) remains uncharacterised. We set out to test the hypothesis that the autonomic nervous system may participate in RAPV via its effect on pulse pressure (PP). Experiments were performed on adult male Sprague-Dawley rats anaesthetised with ketamine and paralysed with pancuronium under positive-pressure ventilation. Respiratory variability in each parameter was quantified by auto-spectral analysis and the relationship between variabilities in two signals assessed by cross-spectral analysis. PP and systolic pressure (SP) exhibited similar powers of respiratory variability that were far more pronounced than for diastolic pressure (DP) or mean pressure (MP). The variability in PP preceded that in SP, MP or DR. The largest phase lag occurred between PP and DP and was equivalent to the time delay of one pulse interval. Coherence between respiratory variabilities in PP and MP was nearly perfect. Propranolol dose dependently suppressed respiratory variability in each pressure parameter and eventually disrupted the PP-MP relationship in respiratory variability. However, the influence of lung volume on MP persisted with a near-zero phase lag. Combined administration of phentolamine and atropine facilitated respiratory variability in PP and SP and failed to block the effect of propranolol. However, the combined administration moved the dose/response curve of propranolol and respiratory variability in each pressure parameter to the right. We conclude that, in addition to non-autonomic mechanisms, RAPV may be facilitated by cardiac sympathetic function via the effect on PP variability. The autonomic mechanism can still be evoked during combined α-adrenoceptor and muscarinic blockade, possibly via baroreflex mechanisms.
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