Vasorelaxant effects of mercury on rat thoracic aorta: The nitric oxide signaling mechanism. (September 2014)

• Record Type: Journal Article
• Authors: Omanwar, S; Saidullah, B; Ravi, K; Fahim, M
• Is Part Of: Human & experimental toxicology. Volume 33:Number 9(2014:Sep.)
• Page Start: 904
• Page End: 910
• Publication Date: 2014-09
• Subjects: Rat aorta -- mercury -- endothelium -- NO -- EDHF -- Ca2+ channels -- oxidative stress; Toxicology -- Periodicals; 615.9
• DOI: 10.1177/0960327113512341
• Languages: English
• ISSNs: 0960-3271

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 ofl -type Ca 2+ channels by generation of free radicals.