A study of the left ventricular systolic pressure response to bilateral changes in carotid sinus pressure was undertaken in which the experimental preparation employed eliminated all parallel and interacting control influences save those of intrasinusal pressures. It was desired to define this physiologic system in terms of three functional blocks, i.e. the baroceptors, the central nervous system (c.n.s.), and the myocardium. The first phase of the study consequently consisted of defining the third, myocardial block, i.e. the systolic pressure response to external simultaneously applied electrical stimulation to both divisions of the autonomic nervous system (a.n.s.). Statistical experimental design procedures were used to derive quadratic regression response surfaces which success-fully described the system's static gain (including sympathetic-parasympathetic negative interactions) as shown by a hybrid computer simulation. The second phase of this work then consisted of measuring and modeling the response of the total carotid sinusmyocardial system, where now the previously defined a.n.s.-myocardial system was used as the final block. A similar experimental preparation was used except that now the inputs consisted of independent pressure sources coupled to each control sinus region. By successively eliminating each autonomic division, it was shown that the systolic pressure response is mediated primarily via the sympathetic division below about 150 mmHg, and primarily by the parasympathetic division above about 150 mmHg of intrasinusal pressure. Statistical comparisons of the effects of left versus right carotid sinus pressure changes showed that the gain of the right sinus is greater than that of the left, and that the response to combined stimulation was greater or lesser than the sum of the individual left and right responses when pressure was decreased or increased, respectively, from a mean value of 150 mmHg. The total system was successfully simulated by means of a hybrid computer, using the above derived model of autonomic-systolic pressure responses as one component. Each component of the overall model was directly identified with its real physiologic component. An interpretation of the derived model structure in physiological terms is briefly discussed.