Nicotine: the link between cigarette smoking and the progression of renal injury?

Nicotine: the link between cigarette smoking and the progression of renal injury? Research Abstract Details 

Research Abstract Table of Contents

Jump to the:

Nicotine: the link between cigarette smoking and the progression of renal injury? Abstract Text:

Edgar A Jaimes,Run-Xia Tian,Leopoldo Raij,

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) alpha4, alpha5, alpha7, beta2, beta3, and beta4. Studies performed in other cell types have shown that these nAChRs are ionotropic receptors that function as agonist-regulated Ca(2+) 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.

Nicotine: the link between cigarette smoking and the progression of renal injury? Publishing Authors By Initials

EA Jaimes,RX Tian,L Raij,

For similar complex mixtures: tars research abstracts see: complex mixtures: tars research

PUBMED ID PMID:

MEDLINE DATE:

Nicotine: the link between cigarette smoking and the progression of renal injury? Journal Published:

PUBLICATION TYPE: Research Support, U.S. Gov't,

Journal: American journal of physiology. Heart and circulat

VOLUME: 292

Page Numbers: H76-82

Journal Abbreviation: Am. J. Physiol. Heart Circ. Ph

ISSN: 0363-6135

DAY: 18

MONTH: 08

YEAR: 2006

Nicotine: the link between cigarette smoking and the progression of renal injury? Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 100901228

Nicotine: the link between cigarette smoking and the progression of renal injury? Keywords Mesh Terms:

KEYWORDS: Tars

MESH TERMS: pharmacology

Chemical & Substance for Abstract: Nicotine: the link between cigarette smoking and the progression of renal injury? Information

Substance Name: Nicotine

Registry Number: 54-11-5

Grant and Affiliation Information for Nicotine: the link between cigarette smoking and the progression of renal injury?

AFFILIATION: VA Medical Center, 1201 NW 16th St., Renal Section, Rm. A-1009, Miami, FL 33125, USA. ejaimes@med.miami.edu

Country: United States

AGENCY: United States NIDDK

GRANT: DK-069372

ACRONYM: DK

MEDLINETA: Am J Physiol Heart Circ Physio

REFSOURCE:

DATABASENAME:

ACCESSION NUMBER:

Number Hits: 0

Nicotine: the link between cigarette smoking and the progression of renal injury? Related Publications

• Dissociation between metabolic and vascular insulin resistance in aging.
• Nicotine: the link between cigarette smoking and the progression of renal injury?
• Nitric oxide and cardiovascular and renal effects.
• Renoprotection by statins is linked to a decrease in renal oxidative stress, TGF-{beta}, and fibronectin with concomitant increase in nitric oxide bioavailability.
• The Angiotensin II Type 2 Receptor: What Is Its Clinical Significance?
• Thiazide diuretics, endothelial function, and vascular oxidative stress.
• Upregulation of cortical COX-2 in salt-sensitive hypertension: role of angiotensin II and reactive oxygen species.
• [In Process Citation]