Oxidative stress, nitric oxide production, and renal sodium handling in leptin-induced hypertension

Bełtowski, Jerzy; Wójcicka, Grażyna; Marciniak, Andrzej; Jamroz, Anna

doi:10.1016/j.lfs.2003.10.029

Cited by 104 publications

(85 citation statements)

References 58 publications

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“…Mechanistically, the regulation of tubular transport by ROS is important to overall salt and water balance and therefore to blood pressure: superoxide stimulates NaCl absorption by the thick ascending limb by activating protein kinase C and by blunting the effects of NO [119]. Hyperleptinemia also induces hypertension, which may be mediated by its stimulation of both systemic and renal oxidative stress, which decreases the amount of bioactive NO and causes renal sodium retention by stimulating tubular sodium resorption [120].…”

Section: E Nox Enzymes and Renal Hypertensionmentioning

confidence: 99%

Nox enzymes, ROS, and chronic disease: An example of antagonistic pleiotropy

Lambeth¹

2007

Free Radical Biology and Medicine

590

454

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Section: E Nox Enzymes and Renal Hypertensionmentioning

confidence: 99%

Nox enzymes, ROS, and chronic disease: An example of antagonistic pleiotropy

Lambeth¹

2007

Free Radical Biology and Medicine

590

454

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“…48 In addition to its effect on sympathetic nervous system to the kidney, leptin may act directly on the kidney to increase oxidative stress, as evidenced by increased plasma concentration and urinary excretion of isoprostanes, increased level of lipid peroxidation products in renal homogenates, and reduced renal aconitase activity in rats treated with leptin. 49 …”

Section: Abnormalities Of Renal Functionmentioning

confidence: 99%

Obesity-Associated Hypertension

et al. 2005

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Abstract-Obesity is strongly associated with hypertension and cardiovascular disease. Several central and peripheral abnormalities that can explain the development or maintenance of high arterial pressure in obesity have been identified. These include activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system. Obesity is also associated with endothelial dysfunction and renal functional abnormalities that may play a role in the development of hypertension. The continuing discovery of mechanisms regulating appetite and metabolism is likely to lead to new therapies for obesity-induced hypertension. Better understanding of leptin signaling in the hypothalamus and the mechanisms of leptin resistance should facilitate therapeutic approaches to reverse the phenomenon of selective leptin resistance. Other hunger and satiety signals such as ghrelin and peptide YY are potentially attractive therapeutic strategies for treatment of obesity and its complications. These recent discoveries should lead to novel strategies for treatment of obesity and hypertension. (Hypertension. 2005;45:9-14.)Key Words: hypertension, obesity Ⅲ nervous system, sympathetic renal Ⅲ vasculature Ⅲ kidney T he increasing prevalence of obesity worldwide is a serious health hazard. This is particularly true for the United States, where Ϸ300 000 deaths each year are associated with being overweight and obese. Obese individuals are at increased risk for diabetes, hypertension, renal failure, and other cardiovascular diseases. Clinical and animal studies have confirmed a strong relationship between obesity and hypertension. 1 Accumulating evidence points to visceral obesity as the most important risk factor for hypertension and cardiovascular disease. 2 Recent work has identified several mechanisms that have therapeutic implications as potential causes of obesity-hypertension. In addition, to these advances, there has also been a revolution in our understanding of neuroendocrine mechanisms regulating appetite, metabolism, and adiposity since the discovery of leptin just Ͼ10 years ago. If, as we predict, these advances soon translate into safe and effective pharmacological treatment of obesity, this would also greatly impact the management of obesityhypertension. Consequently, we briefly review some highlights on advances in understanding the pathophysiology of obesity in addition to highlights on obesity-induced hypertension. New Developments in Neurobiology of ObesityThe identification of leptin represents the most significant breakthrough in obesity research because it helped unravel the architecture of neuroendocrine circuitry that controls appetite and energy homeostasis. Leptin is an adipocyte-derived hormone that acts in the hypothalamus to regulate appetite and energy expenditure. Recently, increasing attention has been dedicated to leptin transduction mechanisms (Figure 1). The leptin receptor is a single transmembrane protein belonging to the cytokine-receptor superfamily known to signal via the janus kinase/signal ...

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“…Apart from the activation of central sympathetic nervous system, leptin actions are referred to the stimulation of endothelin-1 production, but also to blood pressure lowering mechanisms via vasodilation, by promoting nitric oxide release from the endothelium [13]. Moreover, leptin has been found to involve in elevated renal sodium reabsorption, due to increased renal sympathetic nerve activity resulting in high blood pressure [14,15].…”

Section: Discussionmentioning

confidence: 99%

Leptin and hypertension in non-obese patients in renal replacement therapy

Raikou¹,

Kyriaki²

2017

Integr Obesity Diabetes

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Background: The real role of leptin on the vascular disease in end stage of renal disease patients is complicated rather than clear. We considered the relationship between leptin serum concentrations and manifested hypertension in non-obese patients in intermittent dialysis therapy. Methods:We studied 76 patients in on-line hemodiafiltration. Dialysis adequacy was defined by Kt/V for urea. Leptin and i-parathormone (i-PTH) were measured by radioimmunoassay. Metabolic acidosis was determined by serum bicarbonate concentrations less than 22mmol/L. We recorded the home blood pressure according to a standard protocol and it was verified by 24-h monitoring. Antihypertensive treatment was noted. Chi-square tests and adjusted model were performed for the role of leptin on established hypertension.Results: Chi-square tests showed significant association between hypertension and both, low leptin and low bicarbonate (x 2 =12.4, p=0.001 and x 2 =13.1, p=0.001 respectively) and it was supported by the built adjusted model. The patients with hypertension had significantly lower leptin, hemoglobin, normalized protein catabolic rate (nPCR) as a marker of protein intake and bicarbonate levels, but similar dialysis dose than the patients without hypertension. The patients with high leptin had significantly decreased blood pressure, but higher i-PTH, bicarbonate levels and liquids overload in combination with similar dialysis sufficiency comparatively to the patients with low leptin. Conclusion:Hypertension was significantly associated with low leptin in non-obese dialysis patients. In spite of apparently adequate dialysis dose, the involved factors in this relationship may be malnutrition and uncontrolled metabolic acidosis state, although the usage of antihypertensive treatment may play an additional role. Material and Methods SubjectsThis is a dual-center observational cross-sectional study of a cohort of 76 non-obese according to calculated BMI (<25 kg/m 2 ) patients in permanent hemodiafiltration therapy. Patients < 18 years of age at initiation of dialysis treatment, those with less than 6 months of followup, autoimmune diseases, infections, malignancy and patients without regular vascular hemodialysis access and who had dialysis catheter were not included in the study.We enrolled 47 males and 29 females, on mean age 62.2 ± 15 years old, permanently treated by on-line-predilution hemodiafiltration (on-l HDF). The median time in hemodiafiltration treatment was 5 ± interquartile range 3-10 years. The hemodiafiltration treatment was performed 3-times weekly with a dialysis time of 3.5-4 h per session, a Raikou VD (2017) Leptin and hypertension in non-obese patients in renal replacement therapy

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Oxidative stress, nitric oxide production, and renal sodium handling in leptin-induced hypertension

Cited by 104 publications

References 58 publications

Nox enzymes, ROS, and chronic disease: An example of antagonistic pleiotropy

Nox enzymes, ROS, and chronic disease: An example of antagonistic pleiotropy

Obesity-Associated Hypertension

Leptin and hypertension in non-obese patients in renal replacement therapy

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