Effects of Nicotine Exposure on Renal Function of Normal and Hypercholesterolemic Rats

Tamaoki, Lie; Oshiro-Monreal, Fabíola M.; Helou, Claudia M. B.

doi:10.1159/000235622

Cited by 13 publications

(22 citation statements)

References 33 publications

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“…We did not choose Zucker rats to perform the experiments as changes in plasma lipid profiles are associated with obesity, glucose intolerance, hypertension and renal sodium retention in these animals [31]. Hence, we induced hypercholesterolemia by feeding the rats with a high cholesterol diet for 8 days since the animals become hypercholesterolemic with similar body weight, AP and GFR of their control as we have previously reported [15,16]. …”

Section: Discussionmentioning

confidence: 99%

“…We fed the animals with a standard diet (normocholesterolemic rats - NC) or a standard diet supplemented with 4% (w/w) cholesterol and 1% (w/w) cholic acid (hypercholesterolemic rats - HC) [15,16]. Both NC and HC were treated or not with rosiglitazone maleate (Avandia, GlaxoSmithKline, GSK) at a level of 48 mg/kg diet for eight days.…”

Section: Methodsmentioning

confidence: 99%

“…All animals were submitted to the same protocol to evaluate GFR, diuresis, urinary sodium and potassium excretion by measuring inulin clearance as we have previously described [15]. Briefly, we placed catheters in trachea, jugular veins, carotid artery and bladder.…”

Section: Methodsmentioning

confidence: 99%

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Rosiglitazone Did Not Induce Acute Kidney Injury in Normocholesterolemic Rats Despite Reduction in Glomerular Filtration Rate

Dias

Volpini²,

Helou

2013

Kidney Blood Press Res

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Background/Aims: Rosiglitazone (RGL) has been used to ameliorate lipids homeostasis and also to treat inflammatory diseases. However, RGL may reduce renal blood flow and glomerular filtration rate (GFR) predisposing to acute kidney injury (AKI). We investigated whether the treatment with RGL induces AKI in normocholesterolemic (NC) and hypercholesterolemic (HC) rats. Methods: We measured GFR by inulin clearance technique and we quantified urinary neutrophil gelatinase-associated lipocalin (uNGAL) in all groups at baseline and during Ang II-stimulated vasoconstriction. Moreover, we evaluated the presence of renal damaged by histologic examination. Results: At baseline, NC and HC had normal and similar GFR. RGL treatment reduced GFR only in NC+RGL. Unexpectedly, HC+RGL showed high levels of uNGAL although GFR was at normal range. During Ang II-stimulated vasoconstriction, all groups showed reduction in GFR to the same range and we found high levels of uNGAL and high score of renal damage in HC and HC+RGL. Conclusion: RGL acts distinctly in normocholesterolemia and in hypercholesterolemia. Reduction in GFR provoked by RGL treatment did not allow the diagnosis of AKI in NC even in the presence of ANG II-stimulated vasoconstriction. However, AKI was diagnosed in HC+RGL at baseline although GFR was within normal range.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Rosiglitazone Did Not Induce Acute Kidney Injury in Normocholesterolemic Rats Despite Reduction in Glomerular Filtration Rate

Dias

Volpini²,

Helou

2013

Kidney Blood Press Res

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“…For instance, smoking-induced oxidative stress leads to endothelial dysfunction (35) and vascular injury (36). Indeed, studies have found increased renal vascular resistance (11,45), decreased glomerular filtration rate (GFR), and biochemical evidence of smoking or chronic nicotine-induced renal toxicity, even in the absence of histological changes (26). Increased oxidative stress and morphological abnormalities have also been observed in the proximal tubular epithelium after exposure to chronic cigarette smoke or nicotine (NIC) (8 -10, 12), and low-grade damage of proximal tubules has also been observed among chronic smokers in the general population (16,20).…”

mentioning

confidence: 99%

Chronic nicotine exposure exacerbates acute renal ischemic injury

Arany¹,

Grifoni

Clark³

et al. 2011

American Journal of Physiology-Renal Physiology

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Recent epidemiological reports showed that smoking has a negative impact on renal function and elevates the renal risk not only in the renal patient but perhaps also in the healthy population. Studies suggested that nicotine, a major tobacco alkaloid, links smoking to renal dysfunction. While several studies showed that smoking/chronic nicotine exposure exacerbates the progression of chronic renal diseases, its impact on acute kidney injury is virtually unknown. Here, we studied the effects of chronic nicotine exposure on acute renal ischemic injury. We found that chronic nicotine exposure increased the extent of renal injury induced by warm ischemia-reperfusion as evidenced by morphological changes, increase in plasma creatinine level, and kidney injury molecule-1 expression. We also found that chronic nicotine exposure elevated markers of oxidative stress such as nitrotyrosine as well as malondialdehyde. Interestingly, chronic nicotine exposure alone increased oxidative stress and injury in the kidney without morphological alterations. Chronic nicotine treatment not only increased reactive oxygen species (ROS) production and injury but also exacerbated oxidative stress-induced ROS generation through NADPH oxidase and mitochondria in cultured renal proximal tubule cells. The resultant oxidative stress provoked injury through JNK-mediated activation of the activator protein (AP)-1 transcription factor in vitro. This mechanism might exist in vivo as phosphorylation of JNK and its downstream target c-jun, a component of the AP-1 transcription factor, is elevated in the ischemic kidneys exposed to chronic nicotine. Our results imply that smoking may sensitize the kidney to ischemic insults and perhaps facilitates progression of acute kidney injury to chronic kidney injury.

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“…In rats, 100 g/kg of iv nicotine or chronic exposure to oral nicotine resulted in increased arterial BP, decreased GFR, and no change in RBF (22). A lower dose of 2 g·min Ϫ1 ·kg Ϫ1 over 30 min or 2 mg·kg Ϫ1 ·day Ϫ1 for 7 days had no effect on BP or GFR measured by inulin clearance (19).…”

mentioning

confidence: 99%

Nicotine and the kidney: Mr. Hyde, and perhaps some Dr. Jekyll

Budisavljevic

Ploth

2012

American Journal of Physiology-Renal Physiology

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LITERATURE REGARDING THE EFFECTS of smoking on the kidney is rather abundant. However, data assessing the singular effects of nicotine on the kidney are sparse. There are more than 100 substances in tobacco, and nicotine is not a direct cause of most of the tobacco-related diseases (2). Nicotine is, however, highly addictive and as such is, in large part, responsible for the ill effects of smoking. This commentary will focus only on the effects of nicotine on the kidney.Nicotine administered intravenously (iv) at 2 g/kg/min over 10 min results in the exposure equivalent of smoking one cigarette and will result in a nicotine plasma level of 15-20 ng/ml. These and other data suggest a volume of distribution for nicotine equal to or greater than total body water. Although nicotine is absorbed with high efficiency across oral and respiratory membranes, the bioavailability of orally administered nicotine is only 20 -45% (11).One of the earliest reported and still best characterized actions of nicotine is the direct stimulation of release of antidiuretic hormone (ADH), resulting in increased urinary osmolality and decreased free water clearance (3).Studies of the hemodynamic effects of nicotine on kidney function reveal a more complex picture. Early experiments in dogs demonstrated that either iv (1-3 mg) or intrarenal arterial infusion (0.5 g·min Ϫ1 ·kg Ϫ1 over 15 min) of nicotine increased the glomerular filtration rate (GFR), urine volume, and sodium excretion without having a significant effect on fractional excretion of sodium, renal blood flow (RBF), or systemic arterial blood pressure (BP). These effects were attributed to nicotine-induced catecholamine release (3,20

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Effects of Nicotine Exposure on Renal Function of Normal and Hypercholesterolemic Rats

Cited by 13 publications

References 33 publications

Rosiglitazone Did Not Induce Acute Kidney Injury in Normocholesterolemic Rats Despite Reduction in Glomerular Filtration Rate

Rosiglitazone Did Not Induce Acute Kidney Injury in Normocholesterolemic Rats Despite Reduction in Glomerular Filtration Rate

Chronic nicotine exposure exacerbates acute renal ischemic injury

Nicotine and the kidney: Mr. Hyde, and perhaps some Dr. Jekyll

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