Effects of renal denervation on the sodium excretory actions of leptin in hypertensive rats

Villarreal, Daniel; Reams, Garry P.; Freeman, Ronald H.

doi:10.1046/j.1523-1755.2000.00256.x

Cited by 38 publications

(24 citation statements)

References 26 publications

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“…Accordingly, the renal effects of leptin may not only be viewed as the result of plasma hormone level elevation, but also as highly dependent on the underlying regional and systemic hemodynamics, baseline sodium, and water balance. Numerous studies have demonstrated that acute administration of synthetic leptin in the rat produces a significant elevation in urinary sodium and water excretion [14,15,32,34]. Serradeil-Le et al [32] reported that in normal, hydrated, conscious rats intraperitoneal injections of synthetic murine leptin were associated with a significant two-to threefold increase in urinary volume.…”

Section: Leptin and The Kidneymentioning

confidence: 99%

“…The latter hypothesis was examined by a study that evaluated the hemodynamic and renal excretory effects of leptin in anesthetized spontaneously hypertensive rats with either acute or chronic renal denervation [34]. In rats with acute renal denervation, an intravenous bolus of leptin produced a significant two-to fourfold elevation in sodium excretion.…”

Section: Leptin and The Kidneymentioning

confidence: 99%

See 1 more Smart Citation

Leptin: Linking obesity, the metabolic syndrome, and cardiovascular disease

Patel¹,

Reams²,

Spear³

et al. 2008

Current Science Inc

Self Cite

138

102

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The incidence and prevalence of obesity and the metabolic syndrome have risen markedly in the past decade, representing a serious cardiovascular health hazard with significant morbidity and mortality. The etiology of the metabolic syndrome and its various pathogenic mechanisms are incompletely defined and under intense investigation. Contemporary research suggests that the adipocyte-derived hormone leptin may be an important factor linking obesity, the metabolic syndrome, and cardiovascular disorders. Although recent evidence indicates that under normal conditions leptin may be an important factor in regulating pressure and volume, during situations of chronic hyperleptinemia and leptin resistance, this hormone may function pathophysiologically for the development of hypertension and cardiac and renal diseases. Future research will determine if reduction of circulating leptin and/or blockade of its peripheral actions can confer cardiovascular and renal protection in hyperleptinemic patients with obesity and the metabolic syndrome.

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Section: Leptin and The Kidneymentioning

confidence: 99%

Section: Leptin and The Kidneymentioning

confidence: 99%

Leptin: Linking obesity, the metabolic syndrome, and cardiovascular disease

Patel¹,

Reams²,

Spear³

et al. 2008

Current Science Inc

Self Cite

138

102

View full text Add to dashboard Cite

show abstract

“…Dietary-induced obesity is associated with a reduced expression of leptin receptors in the kidney in rats [72] and dogs [73]. Resistance to the natriuretic effect of leptin was observed in SHR [48] and renal denervation restored sensitivity to leptin [74], suggesting an important role of increased renal sympathetic activity. Increased renal SNA is commonly observed in obese animals and humans [75].…”

Section: Selective and Peripheral Leptin Resistancementioning

confidence: 99%

Role of leptin in blood pressure regulation and arterial hypertension

Bełtowski

2006

Journal of Hypertension

191

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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“…These effects are blunted in spontaneously hypertensive rats (SHR) with intact nerves [42,43]. This observation suggests that leptin-mediated stimulation of sympathetic nervous system counteracts the natriuretic effects under normal conditions [44]. An increased sympathetic nerve activity has been recently associated with progression of renal disease [45].…”

Section: Leptin and The Kidneymentioning

confidence: 99%

Leptin and Renal Fibrosis

Wolf

Ziyadeh²

2006

Contributions to Nephrology

168

112

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Leptin is a peptide hormone that is mainly, but not exclusively, produced in adipose tissue and plays a pivotal role in regulating food intake and energy expenditure. Besides its effects on regulation of body weight, appetite and energy expenditure, leptin exhibits influence on the immune system and may contribute to the deterioration of renal function. These direct and indirect renal effects of leptin could partly explain obesity-associated kidney disease and may be also relevant for diabetic nephropathy in type 2 diabetes. Leptin is primarily metabolized in the kidney, presumably by binding to megalin, a multiligand receptor in the proximal tubule, tubular uptake and endocytosis. The kidney expresses abundant concentrations of the small isoform of the leptin receptor (Ob-Ra). In cultured renal rat endothelial cells and mesangial cells obtained from db/db mice, leptin can signal through the Ob-Ra receptor isoform. The peptide stimulates proliferation of glomerular endothelial cells, increases TGF-beta1 synthesis, and collagen type IV production. In contrast, leptin did not influence TGF-beta1 production in mesangial cells, but the peptide stimulates glucose transport in these cells, increased collagen type I synthesis, and lead to an upregulation of surface TGF-beta type II receptors through signal transduction pathways involving phosphatidylinositol-3-kinase. Leptin also stimulates hypertrophy, but not proliferation in cultured rat mesangial cells. Infusion of leptin for 3 weeks into normal rats fosters development of glomerulosclerosis and proteinuria. In addition, transgenic mice with leptin overexpression demonstrated a increase in collagen type IV and fibronectin mRNA in the kidney. Additional previously described direct and indirect effects of leptin on the kidney include natriuretic effects, an increase in sympathetic nervous activity, and stimulation of reactive oxygen species. These findings collectively suggest that the kidney is a target organ for leptin and that this hormone might play an important role in renal pathophysiology.

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Effects of renal denervation on the sodium excretory actions of leptin in hypertensive rats

Cited by 38 publications

References 26 publications

Leptin: Linking obesity, the metabolic syndrome, and cardiovascular disease

Leptin: Linking obesity, the metabolic syndrome, and cardiovascular disease

Role of leptin in blood pressure regulation and arterial hypertension

Leptin and Renal Fibrosis

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