Cigarette Smoking And The Kidneys

Diokine

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My own observations have found that chronic cigarette smoking alters the function of the kidneys, at the local and nervous level. This disruption in the quantitative and qualitative efficiency in the kidneys sets the entire body up for a state of deranged metabolism. The kidneys are critical for maintaining the extracellular environment, which is absolutely necessary for proper anabolic and catabolic functions.




Nicotine exposure and the progression of chronic kidney disease: role of the α7-nicotinic acetylcholine receptor

We determined that the administration of nicotine in the drinking water and at concentrations that result in serum levels similar to those found in the plasma of smokers (16), resulted in increased proteinuria, increased glomerular injury and interstitial fibronectin and TGF-β production, and increased oxidative stress in rats with 5/6Nx.



Nicotine: the link between cigarette smoking and the progression of renal injury?
Cigarette smoke (CS) is the most important source of preventable morbidity and mortality in the United States. Recent clinical studies have suggested that, in addition to being a major cardiovascular risk factor, CS promotes the progression of kidney disease. The mechanisms by which CS promotes the progression of chronic kidney disease have not been elucidated. Here we demonstrate for the first time that human mesangial cells (MCs) are endowed with the nicotinic ACh receptors (nAChRs) α4, α5, α7, β2, β3, and β4. Studies performed in other cell types have shown that these nAChRs are ionotropic receptors that function as agonist-regulated Ca2+channels. Nicotine induced MC proliferation in a dose-dependent manner. At 10 −7 M, a concentration found in the plasma of active smokers, nicotine induced MC proliferation [control, 1,328 ± 50 vs. nicotine, 2,761 ± 90 counts/minute (cpm); P < 0.05] and increased the synthesis of fibronectin (50%), a critical matrix component involved in the progression of chronic kidney disease. We and others have shown that, in response to PKC activation, MC synthesize reactive oxygen species (ROS) via NADPH oxidase. In the current studies we demonstrate that PKC inhibition as well as diphenyleneiodonium and apocynin, two inhibitors of NADPH oxidase, prevented the effects of nicotine on MC proliferation and fibronectin production, hence establishing ROS as second messengers of the actions of nicotine. Furthermore, nicotine increased the production of ROS as assessed by 2′,7′-dichlorofluorescein diacetate fluorescence [control, 184.4 ± 26 vs. nicotine, 281.5 ± 26 arbitrary fluorescence units (AFU); n = 5 experiments, P < 0.05]. These studies unveil previously unrecognized mechanisms that indict nicotine, a component of CS, as an agent that may accelerate and promote the progression of kidney disease.


Prenatal Nicotine Exposure Augments Renal Oxidative Stress in Embryos of Pregnant Rats with Reduced Uterine Perfusion Pressure

Our study demonstrated that maternal nicotine exposure increases renal oxidative stress and consequent (probably sub-lethal) injury in the fetus, especially in combination with placental insufficiency. Since E-cigarettes –that contain pure nicotine– are alarmingly popular (31) and they are perceived as a safe alternative to tobacco use (32)–, their use during pregnancy is potentially increasing. These results call attention to the risk of maternal smoking/nicotine exposure in worsening of renal risk in the growth– restricted fetus.
 

Diokine

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Relevant study relating brain inflammation and alpha-7 acetylcholine receptors

Activation of α7 nicotinic acetylcholine receptor by nicotine selectively up-regulates cyclooxygenase-2 and prostaglandin E2 in rat microglial cultures

Since prostaglandin E2 modulates several macrophage and lymphocyte functions, which are instrumental for inflammatory resolution, our study further supports the existence of a brain cholinergic anti-inflammatory pathway mediated by α7 nicotinic receptor that could be potentially exploited for novel treatments of several neuropathologies in which local inflammation, sustained by activated microglia, plays a crucial role.


 
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