Abstract:
:Mercury, a heavy metal, is widespread and persistent in the environment and has been elucidated as a possible risk factor in cardiovascular diseases. Mercury has been reported to selectively impair the nitric oxide (NO) pathway in the vascular endothelium as a consequence of oxidative stress. Conversely, mercury per se causes endothelium-dependent vasorelaxation at lower concentration via the NO pathway. Little is known about the effects of mercury per se on other endothelial mediators. To elucidate possible mechanisms involved in this action, isometric tension was measured in aortic rings precontracted with phenylephrine (10 µM) from Wistar rats. Responses to increasing concentrations of inorganic mercuric chloride (10(-12)-10(-5) M) were obtained in the presence and absence of endothelium. Inorganic mercury produced a biphasic response in endothelium-intact aortic rings and produced only vasoconstriction in endothelium-denuded aortic rings. To study the possible underlying mechanisms for the biphasic response of mercury, increasing concentrations of mercuric chloride (10(-12)-10(-5) M) were used before and after N(G)-nitro-L-arginine methyl ester (L-NAME (10(-4) M)), glybenclamide (10(-5) M), superoxide dismutase (10 U/ml) + catalase (100 U/ml), and nifedipine (10(-4) M) treatment. Results suggest that mercury produces endothelium-dependent relaxation at low concentration mediated by endothelial-generated NO and endothelium-derived hyperpolarizing factor and endothelium-independent contraction resulting from the blockade of L-type Ca(2+) channels by generation of free radicals.
journal_name
Hum Exp Toxicoljournal_title
Human & experimental toxicologyauthors
Omanwar S,Saidullah B,Ravi K,Fahim Mdoi
10.1177/0960327113512341subject
Has Abstractpub_date
2014-09-01 00:00:00pages
904-10issue
9eissn
0960-3271issn
1477-0903pii
0960327113512341journal_volume
33pub_type
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