Kyungjoon Lim1,2,3, Kristy L Jackson2, Yusuke Sata2,4, Geoffrey A Head5,6,7. 1. Department of Physiology, Anatomy & Microbiology, La Trobe University, Melbourne, VIC, Australia. 2. Neuropharmacology Laboratory, Baker Heart & Diabetes Institute, 75 Commercial Road, Melbourne, VIC, 3004, Australia. 3. Department of Physiology, Monash University, Clayton, VIC, Australia. 4. Central Clinical School, Faculty of Medicine, Nursing and Health Sciences, Monash University, Clayton, VIC, Australia. 5. Neuropharmacology Laboratory, Baker Heart & Diabetes Institute, 75 Commercial Road, Melbourne, VIC, 3004, Australia. Geoff.head@baker.edu.au. 6. Department of Physiology, Monash University, Clayton, VIC, Australia. Geoff.head@baker.edu.au. 7. Department of Pharmacology, Monash University, Clayton, VIC, Australia. Geoff.head@baker.edu.au.
Abstract
PURPOSE OF REVIEW: The major health issue of being overweight or obese relates to the development of hypertension, insulin resistance and diabetic complications. One of the major underlying factors influencing the elevated blood pressure in obesity is increased activity of the sympathetic nerves to particular organs such as the kidney. RECENT FINDINGS: There is now convincing evidence from animal studies that major signals such as leptin and insulin have a sympathoexcitatory action in the hypothalamus to cause hypertension. Recent studies suggest that this may involve 'neural plasticity' within hypothalamic signalling driven by central actions of leptin mediated via activation of melanocortin receptor signalling and activation of brain neurotrophic factors. This review describes the evidence to support the contribution of the SNS to obesity related hypertension and the major metabolic and adipokine signals.
PURPOSE OF REVIEW: The major health issue of being overweight or obese relates to the development of hypertension, insulin resistance and diabetic complications. One of the major underlying factors influencing the elevated blood pressure in obesity is increased activity of the sympathetic nerves to particular organs such as the kidney. RECENT FINDINGS: There is now convincing evidence from animal studies that major signals such as leptin and insulin have a sympathoexcitatory action in the hypothalamus to cause hypertension. Recent studies suggest that this may involve 'neural plasticity' within hypothalamic signalling driven by central actions of leptin mediated via activation of melanocortin receptor signalling and activation of brain neurotrophic factors. This review describes the evidence to support the contribution of the SNS to obesity related hypertension and the major metabolic and adipokine signals.
Entities:
Keywords:
Aversive stress; Blood pressure; Central nervous system; High fat diet; Hypertension; Hypothalamus; Insulin; Leptin; Obesity; Sympathetic nervous system
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