Aluminum exposure for one hour decreases vascular reactivity in conductance and resistance arteries in rats

Journal Article · Thu Dec 15 00:00:00 EST 2016 · Toxicology and Applied Pharmacology

DOI:https://doi.org/10.1016/J.TAAP.2016.10.023· OSTI ID:22690876

Schmidt, Patrícia Medeiros; Escobar, Alyne Goulart; Torres, João Guilherme Dini; Martinez, Caroline Silveira; Rizzetti, Danize Aparecida; Kunz, Simone Noremberg ^[1]; Vassallo, Dalton Valentim ^[2]; Alonso, María Jesús ^[3]; Peçanha, Franck Maciel ^[1]

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1. Postgraduate Program in Biochemistry, Universidade Federal do Pampa, Uruguaiana, Rio Grande do Sul (Brazil)
2. Department of Physiological Sciences, Universidade Federal do Espírito Santo, Espirito Santo (Brazil)
3. Department of Basic Health Sciences, Universidad Rey Juan Carlos, Alcorcón (Spain)

Aims: Aluminum (Al) is an important environmental contaminant; however, there are not enough evidences of Al-induced cardiovascular dysfunction. We investigated the effects of acute exposure to aluminum chloride (AlCl{sub 3}) on blood pressure, vascular reactivity and oxidative stress. Methods and results: Male Wistar rats were divided into two groups: Untreated: vehicle (ultrapure water, ip) and AlCl{sub 3}: single dose of AlCl{sub 3} (100 mg/kg,ip). Concentration-response curves to phenylephrine in the absence and presence of endothelium, the nitric oxide synthase inhibitor L-NAME, the potassium channel blocker tetraethylammonium, and the NADPH oxidase inhibitor apocynin were performed in segments from aortic and mesenteric resistance arteries. NO released was assessed in aorta and reactive oxygen species (ROS), malondialdehyde, non-protein thiol levels, antioxidant capacity and enzymatic antioxidant activities were investigated in plasma, aorta and/or mesenteric arteries. After one hour of AlCl{sub 3} exposure serum Al levels attained 147.7 ± 25.0 μg/L. Al treatment: 1) did not affect blood pressure, heart rate and vasodilator responses induced by acetylcholine or sodium nitroprusside; 2) decreased phenylephrine-induced vasoconstrictor responses; 3) increased endothelial modulation of contractile responses, NO release and vascular ROS production from NADPH oxidase; 4) increased plasmatic, aortic and mesenteric malondialdehyde and ROS production, and 5) decreased antioxidant capacity and affected the antioxidant biomarkers non-protein thiol levels, glutathione peroxidase, glutathione-S-transferase, superoxide dismutase and catalase enzymatic activities. Conclusion: AlCl{sub 3}-acute exposure reduces vascular reactivity. This effect is associated with increased NO production, probably acting on K{sup +} channels, which seems to occur as a compensatory mechanism against Al-induced oxidative stress. Our results suggest that Al exerts toxic effects to the vascular system. - Highlights: • One hour of aluminum exposure decreases vascular reactivity. • Vascular imbalance after aluminum exposure is related to increased oxidative stress. • Enhanced NO release is the first step against the effects of Al at vascular system.

• OSTI ID: 22690876
• Journal Information: Toxicology and Applied Pharmacology, Vol. 313; Other Information: Copyright (c) 2016 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); ISSN 0041-008X
• Country of Publication: United States
• Language: English

Related Subjects

60 APPLIED LIFE SCIENCES
ACETYLCHOLINE
ACUTE EXPOSURE
ALUMINIUM
ALUMINIUM CHLORIDES
ANTIOXIDANTS
AORTA
BIOLOGICAL MARKERS
BLOOD
BLOOD PRESSURE
CATALASE
CONCENTRATION RATIO
ENDOTHELIUM
GLUTATHIONE
HEART
NITRIC OXIDE
OXIDASES
OXIDATION
POTASSIUM IONS
RATS
REACTIVITY
SUPEROXIDE DISMUTASE
THIOLS
TRANSFERASES
VASOCONSTRICTORS
VASODILATORS