PMID- 17159273
OWN - NLM
STAT- MEDLINE
DCOM- 20080208
LR  - 20191210
IS  - 1661-7827 (Print)
IS  - 1660-4601 (Linking)
VI  - 3
IP  - 4
DP  - 2006 Dec
TI  - Cadmium toxicity on arterioles vascular smooth muscle cells of spontaneously 
      hypertensive rats.
PG  - 323-8
AB  - 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.
FAU - Washington, Benny
AU  - Washington B
AD  - Department of Biological Sciences, Tennessee State University, Nashville, TN 
      37209, USA. bwashington@tnstate.edu
FAU - Williams, Shunta
AU  - Williams S
FAU - Armstrong, Patrice
AU  - Armstrong P
FAU - Mtshali, Charlie
AU  - Mtshali C
FAU - Robinson, John T
AU  - Robinson JT
FAU - Myles, Elbert L
AU  - Myles EL
LA  - eng
GR  - RR11808/RR/NCRR NIH HHS/United States
PT  - Evaluation Study
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PL  - Switzerland
TA  - Int J Environ Res Public Health
JT  - International journal of environmental research and public health
JID - 101238455
RN  - 00BH33GNGH (Cadmium)
RN  - EC 2.7.11.13 (Protein Kinase C)
RN  - EC 2.7.12.2 (Mitogen-Activated Protein Kinase Kinases)
SB  - IM
MH  - Animals
MH  - Cadmium/*toxicity
MH  - Cadmium Poisoning/pathology
MH  - Cell Survival/drug effects
MH  - Cells, Cultured
MH  - Dose-Response Relationship, Drug
MH  - Mitogen-Activated Protein Kinase Kinases/metabolism
MH  - Muscle, Smooth, Vascular/*drug effects/enzymology/metabolism
MH  - Myocytes, Smooth Muscle/*drug effects/enzymology/metabolism
MH  - Protein Kinase C/metabolism
MH  - Rats
MH  - Rats, Inbred SHR
EDAT- 2006/12/13 09:00
MHDA- 2008/02/09 09:00
CRDT- 2006/12/13 09:00
PHST- 2006/12/13 09:00 [pubmed]
PHST- 2008/02/09 09:00 [medline]
PHST- 2006/12/13 09:00 [entrez]
AID - 10.3390/ijerph2006030040 [doi]
PST - ppublish
SO  - Int J Environ Res Public Health. 2006 Dec;3(4):323-8. doi: 
      10.3390/ijerph2006030040.