This study evaluates the effect of acute intravenous volume loading on haemodynamics and aortic baroreceptor activity in order to determine the mechanistic factors responsible for divergent heart rate responses to volume loading. Eleven beagles were anaesthetized and instrumented for the recording of aortic pressure, diameter, flow and aortic baroreceptor activity. Isotonic saline, equal to 20% of the estimated blood volume, was infused intravenously within 60-90 s. The animals were divided into tachycardiac and bradycardic groups according to their heart rate response to volume loading. In the group developing the tachycardic response, aortic baroreceptor activity increased. Total peripheral resistance was reduced by 31% and variables representing aortic stretch, mean aortic pressure, diameter and tension remained unchanged. In contrast, in the group developing the bradycardiac response, aortic baroreceptor activity increased markedly. Also in this group peripheral resistance decreased, but only by 15%, which was significantly less than in the tachycardiac group. Factors determining aortic stretch, mean aortic pressure, diameter and tension also increased significantly. Earlier studies show that regardless of the resulting heart rate response, atrial receptor activity increases during volume loading. Thus, we conclude that during cardiac acceleration, marked peripheral vasodilation eliminates the stimulation of baroreceptors and therefore the tachycardic response caused by atrial receptors develops. In the case of cardiac slowing, vasodilation also takes place, but is not sufficient to prevent activation of baroreceptors. In consequence, increased baroreceptor activity overrides the tachycardic drive coming from the atrial receptors and a typical baroreceptor reflex becomes manifested.