Cadmium Toxicity on Arterioles Vascular Smooth Muscle Cells of Spontaneously Hypertensive Rats

Benny Washington, Shunta Williams, Patrice Armstrong, Charlie Mtshali, John T. Robinson and Elbert L. Myles
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Benny Washington: Department of Biological Sciences, Tennessee State University, Nashville, TN 37209, USA
Shunta Williams: Department of Microbiology, Meharry Medical College, Nashville, TN 37208, USA
Patrice Armstrong: Department of Biological Sciences, Tennessee State University, Nashville, TN 37209, USA
Charlie Mtshali: Department of Biological Sciences, Tennessee State University, Nashville, TN 37209, USA
John T. Robinson: Department of Biological Sciences, Tennessee State University, Nashville, TN 37209, USA
Elbert L. Myles: Department of Biological Sciences, Tennessee State University, Nashville, TN 37209, USA

IJERPH, 2006, vol. 3, issue 4, 1-6

Abstract: 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 (CdCl 2 ) 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 CdCl 2 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 CdCl 2 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 ?M CdCl 2 , whereas, 8 and 16 ?M reduced viability by 66±3.1 and 62±4.5% in SHR cells. CdCl 2 increased ERK 1 & 2 in a biphasic manner with maximum increase occurring when cells are exposed to 1 and 4 ?M in SHR VSMCs, whereas, a reduction in ERK 1 and 2 is observed when WKY cells are treated with 2 ?M. The results also indicate that CdCl 2 increased PKC a/ß in both SHR and WKY VSMCs with a greater increase in expression in SHR VSMCs. In addition, the [Ca 2+ ]i chelator, BAPTA, suppressed the CdCl 2 effect, whereas, the PKC inhibitor, GF109203X, reduced the CdCl 2 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.

Keywords: Protein kinase C; mitogen-activated protein kinase; ERK 1; ERK 2; vascular smooth muscle cells (search for similar items in EconPapers)
JEL-codes: I I1 I3 Q Q5 (search for similar items in EconPapers)
Date: 2006
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