Mechanism of alteration in baroreflex cardiovascular responses due to volume loading.

The effect and mechanism of volume loading (VL) on the baroreflex sensitivity, in terms of the changes in arterial pressure (AP) and heart rate (HR) to a given change in carotid sinus pressure (CSP), were studied in rabbits anesthetized with chloralose and urethan. The carotid sinuses were vascularly isolated in order to regulate the CSP independently from the systemic arterial pressure. VL was accomplished by intravenous infusion of dextran solution or whole blood to raise the right atrial pressure from 0.4 to 10 cm water. When the CSP was lowered from 90 to 40 mmHg, VL reduced the baroreflex pressor response by 10.1 mmHg (42%) and 19.9 mmHg (46%) before and after aortic nerves section, respectively. The attenuation effect of VL on the carotid pressor response was abolished after cervical vagotomy. VL also reduced the extent of bradycardia and hypotension upon an elevation of CSP from 90 to 140 mmHg. Before aortic nerve section, the reduction by VL was 19.7 beats/min (41%) for the bradycardic response, and 15.1 mmHg (43%) for the depressor response. These attenuation effects of VL were absent after aortic denervation. The results suggest that VL alters the carotid baroreflex pressor response via the vagal afferents subserving the cardiopulmonary receptors, whereas it reduces the depressor and bradycardic responses through the aortic baroreceptor.