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In usual models of cardiovascular regulation, arterial pressure drives RR interval through a simple baroreflex, and the influence of respiration is dismissed. We examined the applicability of a trivariate autoregressive model to obtain separate values of the gain of the arterial and non-arterial, i.e. cardiopulmonary, components of the lumped baroreflex, employing spontaneous RR interval, systolic arterial pressure and respiration variability.We studied 30 normal subjects (age 37 ± 1 years), both at rest and during standing, a condition known to enhance sympathetic activity while reducing venous return. Electrocardiogram was obtained by telemetry, arterial pressure by Finapres and respiration with a piezoelectric respiratory belt. Data were acquired with a PC and processed with an ad hoc Windows program.We employed an additive and a linear multivariate approach to approximate overall gain of the arterial pressure-heart beat period baroreflex (αlumped) and of its arterial (αart) and non-arterial, i.e. cardiopulmonary (αcp), components, from continuous beat-by-beat series of RR interval, systolic arterial pressure variability and respiration, without using any non-physiological intervention.The overall baroreflex gain at rest (αlumped = 23.7 ± 3.4 ms/mmHg) was subdivided into arterial (αart = 5.2 ± 1.0 ms/mmHg) and cardiopulmonary (αcp = 18.5 ± 3.2ms/mmHg) components. During active orthostatism, αlumped was diminished to 10.0 ± 2.2 ms/ mmHg. In addition, standing selectively reduced αcp to 4.8 ± 1.3 ms/mmHg, while αart was not significantly changed.A trivariate autoregressive model, that considers explicitly the influence of respiration, can subdivide overall, lumped, arterial pressure-heart period baroreflex gain, into two separate components, αart and αcp. Only the latter is reduced by active orthostatism.