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首页> 外文期刊>International Journal of Environmental Research and Public Health >Cadmium Toxicity on Arterioles Vascular Smooth Muscle Cells of Spontaneously Hypertensive Rats
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Cadmium Toxicity on Arterioles Vascular Smooth Muscle Cells of Spontaneously Hypertensive Rats

机译：镉对自发性高血压大鼠小动脉血管平滑肌细胞的毒性

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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 μM CdCl2, whereas, 8 and 16 μM 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 μM in SHR VSMCs, whereas, a reduction in ERK 1 and 2 is observed when WKY cells are treated with 2 μM. The results also indicate that CdCl2 increased PKC a/? 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.
机译：镉（Cd）经常用于各种工业应用中，并且是普遍存在的环境毒物，也存在于烟草烟雾中。暴露的重要途径是循环系统，而血管被认为是Cd毒性的主要器官。我们以前的结果表明，氯化镉（CdCl2）影响高血压大鼠的平均动脉血压。我们假设镉通过镉诱导的MAPKs（ERK 1＆2）的刺激来改变细胞内钙的瞬态机制，这是部分通过钙依赖性PKC机制介导的。为了研究该假设，我们将来自wistar京都（WKY）和自发性高血压大鼠（SHR）的血管平滑肌细胞（VSMC）的原代培养物暴露于浓度升高的CdCl2细胞活力，促分裂原活化蛋白激酶（MAPKs / ERK）表达1和2），以及蛋白激酶C（PKC），它们在几种细胞类型中都被Cd激活。这些研究的结果表明，CdCl2以浓度依赖性方式降低了SHR和WKY VSMC的细胞活力。当暴露于1μMCdCl2时，两种细胞类型的生存力分别降低33±5.3（SHR）和39±2.3 ％（WKY），而8和16μM在SHR细胞中则降低了66±3.1和62±4.5 ％。 CdCl2以双相方式增加ERK 1和2，在SHR VSMC中细胞暴露于1和4μM时发生最大增加，而当WKY细胞用2μM处理时，ERK 1和2减少。结果还表明，CdCl 2增加了PKC a /α。在SHR和WKY VSMC中都有表达，在SHR VSMC中的表达增加更多。此外，[Ca2 +] i螯合剂BAPTA抑制了CdCl2的作用，而PKC抑制剂GF109203X降低了CdCl2对PKC表达的诱导作用。本研究支持以下假设：镉在某些情况下可能是血管平滑肌细胞功能障碍导致高血压的危险因素。

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