The sympathetic nervous system contributes to obesity-related hypertension (reviewed elsewhere). Two recent studies in animals provide concrete evidence for elevated SNA using telemetry to perform chronic sympathetic nerve recordings. Female rats fed a high-caloric, cafeteria-style diet for 15 days display an increase in lumbar SNA as reflected by a greater burst amplitude but not frequency 33. In addition, high-fat feeding in rabbits increases renal SNA 34 through a greater burst amplitude 35. These direct and chronic recordings of SNA corroborate the earlier findings using indirect indices of SNA. However, the “sympathetic signature” of obesity-related hypertension, as suggested by studies on a variety of species, includes elevated renal and/or lumbar (or muscle) SNA but decrease in cardiac SNA frequency 33–35 (reviewed elsewhere 32). The sympathoexcitation in obesity results from multiple factors including leptin and insulin. Intracerebroventricular infusion of leptin or insulin receptor antagonists lowers ABP in high-fat fed rabbits 36. Leptin, but not insulin, receptor blockade reduces renal SNA 36. Moreover, deletion of leptin receptors on specific hypothalamic neuronal populations using transgenic mice also prevents leptin-induced hypertension 37, 38. Parallel experiments with knockdown or deletion of insulin receptors and the impact on obesity-induced hypertension have not yet been performed.
Posters & Accepted Abstracts: Neurological Disorders
Posters & Accepted Abstracts: Neurological Disorders
Scientific Tracks Abstracts: Neurological Disorders
Scientific Tracks Abstracts: Neurological Disorders
Scientific Tracks Abstracts: Neurological Disorders
Scientific Tracks Abstracts: Neurological Disorders
Scientific Tracks Abstracts: Neurological Disorders
Scientific Tracks Abstracts: Neurological Disorders
Posters-Accepted Abstracts: Neurological Disorders
Posters-Accepted Abstracts: Neurological Disorders
Journal of Clinical Neurology and Neurosurgery received 2 citations as per Google Scholar report