Abstract
Although the link between the autonomic nervous system and inflammatory response is well known, it remains unknown how the inflammation affects the baroreflex control of sympathetic nervous activity (SNA). To examine the effect of inflammation on the open-loop static characteristics of the carotid sinus baroreflex, we isolated the bilateral carotid sinuses and controlled intra-sinus pressure (CSP) in Sprague-Dawley rats (380～407 g). Inflammation was induced by intravenous lipopolysaccharide (LPS, 10 mg/kg). Changes in SNA and aortic pressure (AP) in response to CSP input were examined in the presence or the absence of the vagal nerve (N = 4 each). At 3 hours after injection, LPS markedly moved the baroreflex neural arc (CSP-SNA relation) upward by more than 3 times, while shifted the peripheral arc (SNA-AP relation) downward. Vagotomy pronounced these changes with an increase in the peak elevation of TNF-α. In conclusions, LPS-induced inflammation markedly increased SNA via the resetting of the baroreflex neural arc, while decreased the vascular response to SNA. The presence of vagal nerve not only attenuated the inflammatory response but also inhibited sympatho-excitation in the LPS model.
