Obesity does not increase sympathetic vascular tone in hypertensives

Correia, Marcelo; Agapitov, Alexei V.; Sinkey, Christine A.; Mark, Allyn L.; Haynes, William G.

doi:10.1016/j.amjhyper.2005.03.535

Cited by 1 publication

(2 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In fact, such responses were somewhat lower in obese hypertensive subjects than in lean hypertensives. 15 In addition, weight loss did not reduce vasodilator responses to phentolamine in obese hypertensive subjects, despite reducing mSNA and arterial pressure. This is opposite of what would be expected if obesity-related sympathoactivation directly increases limb vascular tone through activation of α-adrenergic receptors on resistance-artery vascular smooth muscle cells.…”

Section: Obesity and Sympathetic Activationmentioning

confidence: 91%

See 1 more Smart Citation

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

2011

View full text Add to dashboard Cite

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.

show abstract

Section: Obesity and Sympathetic Activationmentioning

confidence: 91%

“…This is opposite of what would be expected if obesity-related sympathoactivation directly increases limb vascular tone through activation of α-adrenergic receptors on resistance-artery vascular smooth muscle cells. 16,17 …”

Section: Obesity and Sympathetic Activationmentioning

confidence: 99%