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Mercury effects on the contractile activity of isolated heart muscle
E M Oliveira1, D V Vassallo, J J Sarkis
1Department of Biochemistry, Federal University of Rio Grande do Sul, Porto Alegre, RS, Brazil.
Abstract:
The toxic effects of HgCl2 (1, 2.5, 5, and 10 microM) were studied in isolated, isometrically contracting rat papillary muscles and frog ventricular strips. In rat papillary muscles 1 microM Hg2+ produced a small increase in the force of contraction. Higher concentrations of HgCl2 produced a dose-dependent decrease in contractile force. The rate of force development was affected differently, increasing at 1 and 2.5 microM Hg2+ and decreasing to control levels at 5 and 10 microM Hg2+. This was the result of a progressive reduction in the time to peak tension observed when HgCl2 concentrations increased. This effect probably reflects the binding of Hg2+ to SH groups inducing Ca2+ release from the sarcoplasmic reticulum. The relative potentiation of postrest contractions was used as an index of sarcoplasmic reticulum activity. It was measured after pauses of increasing duration and was reduced at concentrations of 1 microM Hg2+ when compared to that of the control. A further decrement in the relative potentiation was observed with higher Hg2+ concentrations, indicating that the activity of the sarcoplasmic reticulum was depressed by mercury in a dose-dependent manner. Tetanic contractions were also studied in the rat myocardium. The tetanic tension did not change during treatment with 1 microM Hg2+ but decreased with 5 microM Hg2+, suggesting a toxic effect on the contractile proteins only at high Hg2+ concentrations. Frog ventricular strips were studied using the same HgCl2 concentrations and no effects on either force or relative potentiation were observed. These findings suggest that Hg2+ promotes dose-dependent toxic effects on heart muscle via actions on the sarcolemma, the sarcoplasmic reticulum, and contractile proteins.
Insights
Mercury chloride (HgCl2) shows dose-dependent toxic effects on rat heart muscle, impacting contractile force and sarcoplasmic reticulum function. Frog hearts were unaffected, suggesting specific toxicity mechanisms in mammals.
Area of Science:
- Cardiovascular Physiology
- Toxicology
- Cellular Biology
Background:
- Mercury compounds are known environmental toxins.
- Understanding the specific cardiac effects of mercury is crucial for public health.
- Previous research indicates potential cardiovascular impacts of heavy metals.
Purpose of the Study:
- To investigate the dose-dependent toxic effects of mercury(II) chloride (HgCl2) on cardiac muscle.
- To elucidate the mechanisms underlying HgCl2-induced cardiotoxicity in mammalian and amphibian models.
- To assess the impact of Hg2+ on contractility, sarcoplasmic reticulum function, and contractile proteins.
Main Methods:
- Isolated, isometrically contracting rat papillary muscles were exposed to varying HgCl2 concentrations (1-10 microM).
- Frog ventricular strips were subjected to identical HgCl2 treatments.
- Contractile force, rate of force development, post-rest potentiation (sarcoplasmic reticulum index), and tetanic contractions were measured.
Main Results:
- HgCl2 caused a dose-dependent decrease in rat papillary muscle contractile force and altered the rate of force development.
- Sarcoplasmic reticulum activity, assessed by post-rest potentiation, was depressed by HgCl2 in a dose-dependent manner.
- Tetanic tension was unaffected at low HgCl2 concentrations but decreased at higher doses, indicating toxicity to contractile proteins.
- Frog ventricular strips showed no significant effects from HgCl2 exposure.
Conclusions:
- Hg2+ exerts dose-dependent toxic effects on rat heart muscle, targeting the sarcolemma, sarcoplasmic reticulum, and contractile proteins.
- The observed effects suggest that mercury disrupts intracellular calcium handling and direct contractile mechanisms.
- Differential sensitivity between rat and frog cardiac tissue highlights species-specific toxicological responses to mercury.