Abstract
Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous environmental contaminants that are known to increase oxidative stress, proteotoxicity, and cytotoxicity in many cell types, but the acute effects of PAHs on vascular contractility are not known. The 70-kDa heat shock protein (HSP70) is known to protect cells against proteotoxicity and cellular apoptosis. Thus, increased HSP70 may be hypothesized to prevent any negative effects of PAHs on vascular smooth muscle. Heat shock treatment is a method used to increase expression of HSPs. Therefore, the objective of this study was to examine the acute (<24-h) ex vivo effects of a PAH (dimethylbenz[a]anthracene; DMBA), heat shock, or a combination of the two treatments on arterial contractility. The results of the present study suggest that acute ex vivo exposure of rat tail arteries to DMBA caused a transient impairment (at 6 h but not 12 h) in contractile response to norepinephrine (NE), but not to depolarization with excess KCl. The DMBA-induced impairment in NE contraction was not explained by a change in 20-kDa myosin light chain (LC20) phosphorylation. Heat shock alone impaired excess KCl-induced contraction and LC20 phosphorylation. Moreover, heat treatment failed to mitigate the effects of DMBA, suggesting that cytotoxicity was not the mechanism of DMBA effect on NE-induced contractility. Therefore, both acute ex vivo PAH exposure and heat shock impaired contractility of isolated rat tail arteries in the current study but in independent, noninteracting manners.
Published Version
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