Fig. 10.

Hypothesis to explain how insulin can contribute to increased basal sympathetic nerve activity (SNA) and elicit augmented lumbar SNA (LSNA) responses (60) early in obesity development, without normalizing impaired heart rate (HR) baroreflex gain or producing hypertension. Black arrows represent excitatory inputs; gray dashed arrows represent inhibitory inputs. The brain site at which obesity impairs medullary control of parasympathetic nerve activity (PNA) is unknown. ArcN, arcuate nucleus; BBB, blood-brain barrier; BP, blood pressure; CVLM, caudal ventrolateral medulla; α-MSH, α-melanocyte-stimulating hormone; NPY, neuropeptide Y; NTS, nucleus tractus solitarius; POMC, proopiomelanocortin; PVN, paraventricular nucleus; RVLM, rostral ventrolateral medulla; SNA, sympathetic nerve activity. See text for details.