Effects of dietary salt loading on the responses of isolated rat mesenteric arteries to leptin

Jaffar, Mohammed M.; Myers, David S.; Hainsworth, Lucy J.; Hainsworth, R.; Drinkhill, Mark J.

doi:10.1016/j.amjhyper.2004.10.031

Cited by 12 publications

(11 citation statements)

References 16 publications

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“…However, in the setting of obesity, metabolic syndrome and type 2 diabetes -conditions associated with chronic hyperleptinemia -acute depressor effects of leptin are impaired leading to the unbalanced SNS activation and BP elevation (Martin et al 2008). Impairment of the vasodilatory effect of leptin was also observed in rats fed high-salt diet (Jaffar et al 2005) and in spontaneously hypertensive rat (Rodríguez et al 2006). Elucidating the mechanisms of this "vascular leptin resistance" may help in developing novel therapies for arterial hypertension associated with the metabolic syndrome, one of the most common forms of hypertension nowadays.…”

Section: Introductionmentioning

confidence: 94%

Resistance to acute NO-mimetic and EDHF-mimetic effects of leptin in the metabolic syndrome

et al. 2009

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Section: Introductionmentioning

confidence: 94%

Resistance to acute NO-mimetic and EDHF-mimetic effects of leptin in the metabolic syndrome

et al. 2009

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“…Jaffar et al. 46 have shown that leptin induces less marked endothelium‐dependent NO‐mediated relaxation of mesenteric arteries in rats fed a high‐salt diet. Similarly, the ability of leptin to inhibit angiotensin II‐induced contraction of aortic rings is less marked in spontaneously hypertensive rats (SHR) than in normotensive animals 47 .…”

Section: Resistance To the Vascular No‐mimetic Effect Of Leptinmentioning

confidence: 99%

Leptin and the regulation of endothelial function in physiological and pathological conditions

Bełtowski

2012

Clin Exp Pharma Physio

103

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Obesity and the accompanying metabolic syndrome are among the most important causes of cardiovascular pathologies associated with endothelial dysfunction, such as arterial hypertension and atherosclerosis. This detrimental effect of obesity is mediated, in part, by excessive production of the adipose tissue hormone leptin. Under physiological conditions leptin induces endothelium-dependent vasorelaxation by stimulating nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF). Leptin activates endothelial NO synthase (eNOS) through a mechanism involving AMP-activated protein kinase (AMPK) and protein kinase B/Akt, which phosphorylates eNOS at Ser(1177) , increasing its activity. Under pathological conditions, such as obesity and metabolic syndrome, the NO-mediated vasodilatory effect of leptin is impaired. Resistance to the acute NO-mimetic effect of leptin is accounted for by chronic hyperleptinaemia and may result from different mechanisms, such as downregulation of leptin receptors, increased levels of circulating C-reactive protein, oxidative stress and overexpression of suppressor of cytokine signalling-3. In short-lasting obesity, impaired leptin-induced NO production is compensated by EDHF; however, in advanced metabolic syndrome, the contribution of EDHF to the haemodynamic effect of leptin becomes inefficient. Resistance to the vasodilatory effects of leptin may contribute to the development of arterial hypertension owing to unopposed stimulation of the sympathetic nervous system by this hormone.

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“…Nevertheless, subthreshold concentrations of insulin augment the effect of leptin on Akt phosphorylation, eNOS phosphorylation and NO release [33]. Recently, it was demonstrated that feeding rats a highsalt diet for 1 month attenuates the vasodilatory NOdependent effect of leptin on isolated mesenteric arteries [34].…”

Section: Leptin and Nitric Oxidementioning

confidence: 99%

Role of leptin in blood pressure regulation and arterial hypertension

Bełtowski

2006

Journal of Hypertension

192

123

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Leptin is a 16-kDa protein secreted by white adipose tissue that is primarily involved in the regulation of food intake and energy expenditure. Plasma leptin concentration is proportional to the amount of adipose tissue and is markedly increased in obese individuals. Recent studies suggest that leptin is involved in cardiovascular complications of obesity, including arterial hypertension. Acutely administered leptin has no effect on blood pressure, probably because it concomitantly stimulates the sympathetic nervous system and counteracting depressor mechanisms such as natriuresis and nitric oxide (NO)-dependent vasorelaxation. By contrast, chronic hyperleptinemia increases blood pressure because these acute depressor effects are impaired and/or additional sympathetic nervous system-independent pressor effects appear, such as oxidative stress, NO deficiency, enhanced renal Na reabsorption and overproduction of endothelin. Although the cause-effect relationship between leptin and high blood pressure in humans has not been demonstrated directly, many clinical studies have shown elevated plasma leptin in patients with essential hypertension and a significant positive correlation between leptin and blood pressure independent of body adiposity both in normotensive and in hypertensive individuals. In addition, leptin may contribute to end-organ damage in hypertensive individuals such as left ventricular hypertrophy, retinopathy and nephropathy, independent of regulating blood pressure. Here, current knowledge about the role of leptin in the regulation of blood pressure and in the pathogenesis of arterial hypertension is presented.

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Effects of dietary salt loading on the responses of isolated rat mesenteric arteries to leptin

Cited by 12 publications

References 16 publications

Resistance to acute NO-mimetic and EDHF-mimetic effects of leptin in the metabolic syndrome

Resistance to acute NO-mimetic and EDHF-mimetic effects of leptin in the metabolic syndrome

Leptin and the regulation of endothelial function in physiological and pathological conditions

Role of leptin in blood pressure regulation and arterial hypertension

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