-The cardiopulmonary baroreflex responds to an increase in central venous pressure (CVP) by decreasing total peripheral resistance and increasing heart rate (HR) in dogs. However, the direction of ventricular contractility change is not well understood. The aim was to elucidate the cardiopulmonary baroreflex control of ventricular contractility during normal physiological conditions via a mathematical analysis. Spontaneous beat-to-beat fluctuations in maximal ventricular elastance (E max), which is perhaps the best available index of ventricular contractility, CVP, arterial blood pressure (ABP), and HR were measured from awake dogs at rest before and after -adrenergic receptor blockade. An autoregressive exogenous input model was employed to jointly identify the three causal transfer functions relating beat-to-beat fluctuations in CVP to E max (CVP ¡ Emax), which characterizes the cardiopulmonary baroreflex control of ventricular contractility, ABP to E max, which characterizes the arterial baroreflex control of ventricular contractility, and HR to E max, which characterizes the force-frequency relation. The CVP ¡ E max transfer function showed a static gain of 0.037 Ϯ 0.010 ml Ϫ1 (different from zero; P Ͻ 0.05) and an overall time constant of 3.2 Ϯ 1.2 s. Hence, E max would increase and reach steady state in ϳ16 s in response to a step increase in CVP, without any change to ABP or HR, due to the cardiopulmonary baroreflex. Following -adrenergic receptor blockade, the CVP ¡ E max transfer function showed a static gain of 0.0007 Ϯ 0.0113 ml Ϫ1 (different from control; P Ͻ 0.10). Hence, E max would change little in steady state in response to a step increase in CVP. Stimulation of the cardiopulmonary baroreflex increases ventricular contractility through -adrenergic receptor system mediation.beat-to-beat variability; cardiopulmonary baroreflex; maximal ventricular elastance; system identification; ventricular contractility THE BAROREFLEX SYSTEMS ARE primarily responsible for maintaining blood pressure in the short term (seconds to minutes) and also appear to contribute to longer-term blood pressure regulation (29,30). It is well known that the arterial baroreflex senses arterial blood pressure (ABP) via stretch receptors lying in the carotid sinus and aortic arch and buffers an increase in ABP by decreasing, for example, total peripheral resistance (TPR), heart rate (HR), and ventricular contractility. The sensory receptors of the cardiopulmonary baroreflex are more complex, residing mainly in the cardiac chambers but also in the pulmonary vessels (5). These receptors have been shown to be responsive to both central venous pressure (CVP) (7,25) and left atrial pressure (LAP) (10, 21), which often change in parallel. The cardiopulmonary baroreflex responds to a change in these pressures by inducing an opposite change in TPR (1,16,25). An increase in the preload pressures also leads to an increase in HR (i.e., Bainbridge effect) in dogs (3), but an opposite change may occur in humans (7).However, the cardiopulmon...