Catecholamine neurons in the rostral ventrolateral medulla (RVLM) contribute to the cardiovascular effects of endotoxin challenge

Abstract

The rostral ventrolateral medulla (RVLM) is critical to neural control of cardiovascular function. Spinally‐projecting sympathoexcitatory RVLM neurons can be divided into two groups: C1 neurons that express catecholamine biosynthetic enzymes, and non‐C1 neurons that do not. Selective lesioning of RVLM‐C1 neurons in rats with saporin conjugated to an antibody against dopamine beta‐hydroxylase has provided evidence that C1 neurons contribute to cardiovascular reflexes, homeostatic responses to glucoprivation, pressor responses to restraint stress, and other sympathoexcitatory responses. We hypothesized that C1 neurons also play a role in cardiovascular responses to interoceptive stress induced by injection of endotoxin (lipopolysaccharide; LPS), a fragment of gram‐negative bacterial cell walls that presents an immune challenge by stimulating the release of pro‐inflammatory cytokines. Radiotelemetry transmitters were used to record blood pressure (BP) and heart rate (HR) in conscious rats after LPS challenge (200 ug/kg, i.p.). In rats with substantial loss of C1 neurons, BP was attenuated throughout the biphasic pressor response to LPS, and both HR and HR variability response patterns were altered. These data provide further support for an important role of RVLM‐C1 neurons in mediating sympathoexcitatory cardiovascular responses to homeostatic challenges. (Supported by HL55786 and MH59911).