Exposure to low mercury concentration in vivo impairs myocardial contractile function

Journal Article · Thu Sep 01 00:00:00 EDT 2011 · Toxicology and Applied Pharmacology

DOI:https://doi.org/10.1016/j.taap.2011.06.015· OSTI ID:21587831

Furieri, Lorena Barros; Fioresi, Mirian; Junior, Rogerio Faustino Ribeiro ^[1]; Bartolome, Maria Visitacion ^[2]; Fernandes, Aurelia Araujo ^[1]; Cachofeiro, Victoria; Lahera, Vicente ^[2]; Salaices, Mercedes ^[3]; Stefanon, Ivanita ^[1]

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1. Department of Physiological Sciences, Federal University of Espirito Santo, Vitoria, ES (Brazil)
2. Department of Physiology, Universidad Complutense de Madrid (Spain)
3. Department of Pharmacology, Universidad Autonoma de Madrid (Spain)

Increased cardiovascular risk after mercury exposure has been described but cardiac effects resulting from controlled chronic treatment are not yet well explored. We analyzed the effects of chronic exposure to low mercury concentrations on hemodynamic and ventricular function of isolated hearts. Wistar rats were treated with HgCl{sub 2} (1st dose 4.6 {mu}g/kg, subsequent dose 0.07 {mu}g/kg/day, im, 30 days) or vehicle. Mercury treatment did not affect blood pressure (BP) nor produced cardiac hypertrophy or changes of myocyte morphometry and collagen content. This treatment: 1) in vivo increased left ventricle end diastolic pressure (LVEDP) without changing left ventricular systolic pressure (LVSP) and heart rate; 2) in isolated hearts reduced LV isovolumic systolic pressure and time derivatives, and {beta}-adrenergic response; 3) increased myosin ATPase activity; 4) reduced Na{sup +}-K{sup +} ATPase (NKA) activity; 5) reduced protein expression of SERCA and phosphorylated phospholamban on serine 16 while phospholamban expression increased; as a consequence SERCA/phospholamban ratio reduced; 6) reduced sodium/calcium exchanger (NCX) protein expression and {alpha}-1 isoform of NKA, whereas {alpha}-2 isoform of NKA did not change. Chronic exposure for 30 days to low concentrations of mercury does not change BP, heart rate or LVSP but produces small but significant increase of LVEDP. However, in isolated hearts mercury treatment promoted contractility dysfunction as a result of the decreased NKA activity, reduction of NCX and SERCA and increased PLB protein expression. These findings offer further evidence that mercury chronic exposure, even at small concentrations, is an environmental risk factor affecting heart function. - Highlights: > Unchanges blood pressure, heart rate, systolic pressure. > Increases end diastolic pressure. > Promotes cardiac contractility dysfunction. > Decreases NKA activity, NCX and SERCA, increases PLB protein expression. > Small concentrations constitutes environmental cardiovascular risk factor.

• OSTI ID: 21587831
• Journal Information: Toxicology and Applied Pharmacology, Vol. 255, Issue 2; Other Information: DOI: 10.1016/j.taap.2011.06.015; PII: S0041-008X(11)00237-7; Copyright (c) 2011 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
BLOOD PRESSURE
CHRONIC EXPOSURE
COLLAGEN
DOSES
HAZARDS
HEART
IN VIVO
MERCURY
MERCURY CHLORIDES
MYOSIN
RATS
ANIMALS
BODY
CARDIOVASCULAR SYSTEM
CHLORIDES
CHLORINE COMPOUNDS
ELEMENTS
GLOBULINS
HALIDES
HALOGEN COMPOUNDS
MAMMALS
MERCURY COMPOUNDS
MERCURY HALIDES
METALS
ORGANIC COMPOUNDS
ORGANS
PROTEINS
RODENTS
SCLEROPROTEINS
VERTEBRATES