Aim The baroreflex is a key mechanism in cardiovascular regulation, and alterations in baroreceptor function are seen in many diseases, including heart failure, obesity and hypertension. We propose a new method for analysing baroreceptor function from continuous blood pressure (BP) and heart rate (HR) in both health and disease. Methods Forty‐eight‐hour data series of BP and HR were collected with telemetry. Sprague Dawley rats on standard chow (n = 11) served as controls, while rats on a high‐fat, high‐fructose (HFHC) diet (n = 6) constituted the obese‐hypertensive model. A third group of rats underwent autonomic blockade (n = 6). An autoregressive–moving‐average with exogenous inputs (ARMAX) model was applied to the data and compared with the α‐coefficient. Results Autonomic blockade caused a significant reduction in the strength of the baroreflex as estimated by ARMAX [ARMAX‐ baroreflex sensitivity (BRS)] −0.03 ± 0.01 vs. −0.19 ± 0.04 bpm heartbeat−1). Both methods showed a ~50% reduction in BRS in the obese‐hypertensive group compared with control (body weight 531 ± 27 vs. 458 ± 19 g, P < 0.05; mean arterial pressure 119 ± 3 vs. 102 ± 1 mmHg, P < 0.05; ARMAX‐BRS −0.08 ± 0.01 vs. −0.15 ± 0.01 bpm heartbeat−1, P < 0.05; α‐coefficient BRS 0.51 ± 0.07 vs. 0.89 ± 0.07 ms mmHg−1, P < 0.05). The ARMAX method additionally showed the open‐loop gain of the baroreflex to be reduced by ~50% in the obese‐hypertensive group (−2.3 ± 0.3 vs. −4.1 ± 0.3 bpm, P < 0.05), while the rate constant was similar between groups. Conclusion The ARMAX model represents an efficient method for estimating several aspects of the baroreflex. The open‐loop gain of the baroreflex was attenuated in obese‐hypertensive rats compared with control, while the time response was similar. The algorithm can be applied to other species including humans.