Document Detail

Cadmium toxicity on arterioles vascular smooth muscle cells of spontaneously hypertensive rats.
MedLine Citation:
PMID:  17159273     Owner:  NLM     Status:  MEDLINE    
Cadmium (Cd) is frequently used in various industrial applications and is a ubiquitous environmental toxicant, also present in tobacco smoke. An important route of exposure is the circulatory system whereas blood vessels are considered to be main stream organs of Cd toxicity. Our previous results indicate that cadmium chloride (CdCl2) affects mean arterial blood pressure in hypertensive rats. We hypothesized that Cd alters the intracellular calcium transient mechanism, by cadmium-induced stimulation of MAPKs (ERK 1 & 2) which is mediated partially through calcium-dependent PKC mechanism. To investigate this hypothesis, we exposed primary cultures of vascular smooth muscle cells (VSMCs) from wistar kyoto (WKY) and spontaneously hypertensive rats (SHR) to increased concentrations of CdCl2 on cell viability, expression of mitogen-activated protein kinases (MAPKs/ERK 1 & 2), and protein kinase C (PKC) which are activated by Cd in several cell types. The results from these studies indicate that CdCl2 decreased cell viability of both SHR and WKY VSMCs in a concentration dependent-manner. Viability of both cell types decreased 33+/-5.3 (SHR) and 39+/-2.3% (WKY) when exposed to 1 microM CdCl2, whereas, 8 and 16 microM reduced viability by 66+/-3.1 and 62+/-4.5% in SHR cells. CdCl2 increased ERK 1 & 2 in a biphasic manner with maximum increase occurring when cells are exposed to 1 and 4 muM in SHR VSMCs, whereas, a reduction in ERK 1 and 2 is observed when WKY cells are treated with 2 microM. The results also indicate that CdCl2 increased PKC a/Beta in both SHR and WKY VSMCs with a greater increase in expression in SHR VSMCs. In addition, the [Ca2+]i chelator, BAPTA, suppressed the CdCl2 effect, whereas, the PKC inhibitor, GF109203X, reduced the CdCl2 induced-effect on PKC expression. The present studies support the hypothesis that Cd can be a risk factor of hypertension through dysfunction of vascular smooth muscle cells under certain conditions.
Benny Washington; Shunta Williams; Patrice Armstrong; Charlie Mtshali; John T Robinson; Elbert L Myles
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Publication Detail:
Type:  Evaluation Studies; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  International journal of environmental research and public health     Volume:  3     ISSN:  1661-7827     ISO Abbreviation:  Int J Environ Res Public Health     Publication Date:  2006 Dec 
Date Detail:
Created Date:  2006-12-12     Completed Date:  2008-02-08     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  101238455     Medline TA:  Int J Environ Res Public Health     Country:  Switzerland    
Other Details:
Languages:  eng     Pagination:  323-8     Citation Subset:  IM    
Department of Biological Sciences, Tennessee State University, Nashville, TN 37209, USA.
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MeSH Terms
Cadmium / toxicity*
Cadmium Poisoning / pathology
Cell Survival / drug effects
Cells, Cultured
Dose-Response Relationship, Drug
Mitogen-Activated Protein Kinase Kinases / metabolism
Muscle, Smooth, Vascular / drug effects*,  enzymology,  metabolism
Myocytes, Smooth Muscle / drug effects*,  enzymology,  metabolism
Protein Kinase C / metabolism
Rats, Inbred SHR
Grant Support
Reg. No./Substance:
7440-43-9/Cadmium; EC Kinase C; EC Protein Kinase Kinases

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