Abstract
Diet‐induced obesity elevates sympathetic nerve activity (SNA) and arterial blood pressure (ABP). PVN neurons influence SNA and ABP through mono‐ and poly‐synaptic projections to the brainstem and spinal cord. The purpose of the present study was to determine whether PVN neurons contribute to elevated SNA and ABP in diet‐induced obesity. Male Sprague‐Dawley rats (250–300g) were placed on a low‐fat (LF) or moderate high‐fat diet for 15 weeks and segregated into obesity‐resistant (OR) and obesity‐prone (OP) groups. OP versus OR or low‐fat rats had a significantly higher body weight (OP: 774±7g, OR: 630±7g, LF: 607±8g, n=6 per group) and adiposity (OP: 7.8±0.4%, OR: 5.6±0.5%, LF: 4.4±0.6%). Inhibition of PVN neurons by bilateral microinjection of glycine (0.5M/60nL/side) produced a significantly greater fall in lumbar SNA (OP: −15±3%, OR: −7±1%, LF: −5±2%, P<0.05) and mean ABP OP: −12±3mmHg, OR: − 6±2mmHg, LF: −6±1mmHg, P<0.05) but not splanchnic SNA (OP: −2±2%, OR: −2±2%, LF: 1±1%). Inhibition of PVN neurons with the GABAA agonist muscimol (2mM/60nL/side) produced similar responses. A linear regression analysis revealed a significant correlation between adiposity and the glycine‐induced fall in lumbar SNA (r=0.462) and mean ABP (r=0.525) but not splanchnic SNA (0.046). These findings suggest PVN neurons contribute to obesity‐induced sympathoexcitation and hypertension.
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