Weight loss does not alter sympatheticatly-mediated vascular tone in normotensive obese humans

Agapitov, Alexei V.; Correia, Marcelo; Dopp, John M.; Sinkey, Christine A.; Phillips, Brian N.; Haynes, William G.

doi:10.1016/s0735-1097(02)81202-5

Cited by 2 publications

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“…We have shown that orlistat decreases sympathetic nerve traffic by 20% in obese normotensive 139 and by 26% in obese hypertensive subjects. 140 Most patients have sustained weight loss with orlistat, with a ‘failure’ rate (defined as < 5% weight loss at 12 months) of 51% compared with 77% for placebo.…”

Section: Therapeutic Implicationsmentioning

confidence: 79%

Sympathetic nervous system in obesity-related hypertension: mechanisms and clinical implications

2011

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Obesity markedly increases the risk of hypertension and cardiovascular disease, which may be related to activation of the sympathetic nervous system (SNS). Sympathetic overactivity directly and indirectly contributes to blood pressure (BP) elevation in obesity, including stimulation of the renin–angiotensin–aldosterone system (RAAS). The adipocyte-derived peptide leptin suppresses appetite, increases thermogenesis, but also raises SNS activity and BP. Obese individuals exhibit hyperleptinemia but are resistant to its appetite-suppressing actions. Interestingly, animal models of obesity exhibit preserved sympathoexcitatory and pressor actions of leptin, despite resistance to its anorexic and metabolic actions, suggesting selective leptin resistance. Disturbance of intracellular signaling at specific hypothalamic neural networks appears to underlie selective leptin resistance. Delineation of these pathways should lead to novel approaches to treatment. In the meantime, treatment of obesity–hypertension has relied on antihypertensive drugs. Although sympathetic blockade is mechanistically attractive in obesity–hypertension, in practice its effects are disappointing because of adverse metabolic effects and inferior outcomes. On the basis of subgroup analyses of obese patients in large randomized clinical trials, drugs such as diuretics and RAAS blockers appear superior in preventing cardiovascular events in obesity–hypertension. An underused alternative approach to obesity–hypertension is induction of weight loss, which reduces circulating leptin and insulin, partially reverses resistance to these hormones, decreases sympathetic activation and improves BP and other risk factors. Though weight loss induced by lifestyle is often modest and transient, carefully selected pharmacological weight loss therapies can produce substantial and sustained antihypertensive effects additive to lifestyle interventions.

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Section: Therapeutic Implicationsmentioning

confidence: 79%

Sympathetic nervous system in obesity-related hypertension: mechanisms and clinical implications

2011

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“…However, the results of a preliminary study suggest that this does not appear to be the case nor is sympathetic vasoconstrictor tone reduced with weight loss in obese humans [48]. The relatively normal sympathetic vasoconstrictor tone might be the result of a correspondingly lower rate of norepinephrine spillover to skeletal muscle in obesity [13].…”

Section: Potential Consequences Of Sympathetic Nervous System Activatmentioning

confidence: 94%

The global epidemic of obesity: Are we becoming more sympathetic?

Davy

2004

Current Science Inc

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The relationship between obesity and sympathetic nervous system (SNS) behavior has been controversial. Existing paradigms have been opposed in their views of the directional changes in SNS activity in obesity. In addition, limitations of previous approaches to assess SNS activity have produced inconsistent findings. However, the use of state-of-the-art neurochemical and neurophysiologic techniques has improved our current understanding of this issue. There is regional heterogeneity in the SNS activation associated with obesity, with the renal and skeletal muscle circulations, but not the heart, being targets for SNS activation. Abdominal visceral fat appears to be an important depot linking obesity and skeletal muscle SNS activation. The impact of this depot on SNS activity to the kidney or other regions is unknown. Future studies are needed to address this issue as well as the mechanisms and consequences of SNS activation in visceral obesity.

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Weight loss does not alter sympatheticatly-mediated vascular tone in normotensive obese humans

Cited by 2 publications

References 0 publications

Sympathetic nervous system in obesity-related hypertension: mechanisms and clinical implications

Sympathetic nervous system in obesity-related hypertension: mechanisms and clinical implications

The global epidemic of obesity: Are we becoming more sympathetic?

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