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The Effects of Acute Treatment with Low Doses of Arsenic on Vasoconstrictor and Vasodilator Responses of Thoracic Aorta from Rats
Author(s) -
Brooks Kanesha M,
RodriguezAlvarez Walter E,
Fleming John T,
Joshua Irving G
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.976.4
Subject(s) - sodium nitroprusside , phenylephrine , arsenic , vasodilation , vasoconstriction , nitric oxide , acetylcholine , chemistry , endocrinology , medicine , aorta , pharmacology , blood pressure , organic chemistry
Exposure to arsenic is correlated with the development of cardiovascular diseases such as hypertension. The objective of the present study was to determine if acute exposure to low levels of arsenic induced dysfunction in the vasomotor responses of blood vessels. The effects of acute exposure to arsenic on vasorelaxation and vasoconstriction were investigated using isolated aortic rings from Sprague‐Dawley rats. The rings were pre‐treated with two concentrations of arsenic (5 and 10μM) for one hour. Then the aortic rings were exposed to increasing concentrations of phenylephrine, acetylcholine, or sodium nitroprusside. After one‐hour treatment with one of the two levels of arsenic (5 and 10 μM) the acetylcholine‐induced relaxation was significantly attenuated (33% and 44%, respectively) while the sodium nitroprusside‐induced relaxation was unaltered. After exposure to 5 and 10 μM arsenic the maximal constriction responses to phenylephrine increased by 25% and 17%, respectively. These in vitro results indicate that arsenic is capable of increasing the maximal contraction response to alpha‐adrenergic receptor stimulation and this increased response may be related to impaired endothelial cells production of nitric oxide.