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TOXIC EFFECTS OF MERCURY ON BLOOD PRESSURE AND MYOCARDIAL CONTRACTILITY

Received on 22 December 2016

Abstract

Environmental contamination by heavy metals such as mercury (Hg), cadmium (Cd) and lead (Pb) has exposed humans producing health consequences. Mercury actions are remarkable in this context, due to its high toxicity and high mobility in ecosystems promoting toxicity to many organs and tissues of our body and the health consequences of such exposure are not clearly understood. Mercury have been used for many years in a wide variety of human activities, and nowadays both natural and artificial sources are significantly increasing the exposure to this metal. Several studies show that mercury exposure induces changes in the cardiovascular system, such as hypertension in humans and animals. In isolated myocardium preparations mercury in uM concentrations produces a positive inotropic effect followed by a toxic effect with negative inotropism at higher concentrations. The metal produces potent reducing effect of myosin ATPase activity, and in isolated hearts, promotes reduction of the developed pressure, heart rate and increases the incidence of arrhythmias. On the vessels produced important peripheral and pulmonary vasoconstriction. In anesthetized animals it also lowers blood pressure and causes bradycardia. The blood pressure reduction is due to the development of diastolic heart failure and pulmonary hypertension. In recent years we have focused efforts on the same preparations using nanomolar concentrations of mercury. These concentrations have shown, after some time, toxic effects explained by the fact that the cells concentrated mercury. Moreover, under chronic exposure with mercury for 30 days the cardiovascular effects showed: no increase in blood pressure; hemodynamic parameters showed a single change, the increased left ventricle end diastolic pressure; in isolated hearts we observed reduction of developed pressure and time derivatives at baseline conditions and in almost all studied diastolic pressures, and decreased β-adrenergic response; the treatment do not change the contractile parameters in left ventricle papillary muscles but increased the activity of myosin Ca2+-ATPase and inhibited the specific activity of Na,K-ATPase; and occurs coronary endothelial dysfunction by increased production of free radicals. The results described in this review indicate that mercury exposure, even at low doses, affects cardiovascular function. As a result, the reference values defining the limits for the absence of danger should be reduced. The results described in this review indicate that mercury exposure, even at low doses, affects cardiovascular function. As a result, the reference values defining the limits for the absence of danger should be reduced.

Introduction

The use of heavy metals has intimate connection to the history of man. Since prehistoric tools. However, the records relating to metals are not only those who report their benefits. Heavy metals such as mercury (Hg), cadmium (Cd) and lead (Pb) are environmental contaminants and toxic to many organs and tissues of our body.12,30 Mercury actions are remarkable in this context, due to its high toxicity and high mobility in ecosystems.36

Mercury has been used commercially and in medicine for centuries. In the past, several drugs commonly constituted several medicines and today it is still the primary use to preserve vaccines. Even with the knowledge of its toxicity, to a lesser extent, it is still being used in hospital equipments, such as thermometers and sphygmomanometers and commercially, in fluorescent lamps and batteries. Thus, its use leads both to accidental                                      and occupational exposure.13 Many organomercury compounds were used as pesticides (eventually in an inadvisable form are still employed), others follow with medical applications as an antiseptic (such as the sodium salt of o-ethylmercury acid, commercially known as Merthiolate), and also the metal have been used as mercurial diuretics (Azevedo, 2003).

Mercury is absorbed in the form of vapor (via the pulmonary route) through the gastro-intestinal tract (oral ingestion, soluble form) or through the skin and sebaceous glands (insoluble form), distributing and accumulating in almost all organs and tissues of our body.11,38 The most common chemical forms, which enable these modes of absorption are as HgCl2, which is soluble in water, the methyl mercury, which is well absorbed by the digestive tract and which commonly accumulates in animals as fishes (hence the absorption by human beings eating these animals) and metallic mercury (which generates vapors or aerosols) can be absorbed due to its high lipid solubility. After absorption Hg concentrates mainly in kidneys and nervous tissue. Its effects are already known on the central nervous system, promoting serious and irreversible damage; on the kidney promoting tubular and glomerular lesions; on the intestines (caustic action of Hg responsible for acute digestive disorders), causing severe diarrhea by intestinal mucosal injury as well as toxic effects on other organs and tissues (chronic hidroargirism). Chronic mercury poisoning comes from the absorption of small quantities over prolonged periods of time, usually as a result of occupational exposure.

Whereas mercury can be concentrated within the cells, with higher intracellular concentrations than in plasma,11 our purpose is to describe a series of experimental results about the acute and chronic effects of concentrations observed in individuals exposed to the metal , as those obtained after removal of amalgam fillings on the cardiovascular system, given that today, mercury is widely used in industrial products, various techniques and can be accumulated in food or absorbed in different ways, in the industries of extraction.

The EPA17 (US Environmental Protection Agency’s 1997) recommends mercury reference value in blood being the exposure considered without adverse effect of 5.8 ng/mL (~21,6 nM)24,37,40 and estimates that each release dental amalgam attains 3 to 17 µg of mercury vapor per day. In individuals with amalgam restoration inorganic mercury concentration in blood is about 4.3 ng/mL (~ 16 nM).49 People with more than six amalgam restorations have an average of 2.3 ug Hg/g of tissue8 and may reach in some cases, at 380 ug Hg/g.20 The blood concentration, reported in non-exposed population is about 3 ng / ml (~ 11 nM)53 and studies of workers exposed to mercury found blood concentration of mercury 10.8 ± 1.3 ng/mL (~39,6nM) and 1.6 ± 0.2 ng/mL in control subjects.25 Serum levels in residents of Guizhou province in China, a typical contaminated area was 7.5 ± 3.2 ng/mL (27.5 nM~) while in unexposed individuals was 0.91 ± 0.3 ng/mL.10 Spanish children, consumers of a diet with fish have mercury concentration in the hair three times higher when compared to children who do not consume fish (1.4 ng/g vs 0.49 ng/g), a concentration which was more than that recommended by EPA (1 ng/g).16 In the population living in the Amazon basin and using fish as the primary protein feeding source the mercury concentrations in the hair came up to 150 mg/g, and only 2 of 40 studied municipalities have the average mercury concentration below that recommended by the WHO.4 The WHO considers a concentration lower than 6 g/g of mercury as acceptable in human hair.53

The functional changes promoted by mercury are often accompanied by changes in one or more processes involved in the excitation-contraction coupling mechanism as: 1) inhibition of the Na+ – K+-ATPase.1,2 2) inhibition of Ca2+ myosin-ATPase.35 3) inhibition of the calcium pump of the sarcoplasmic reticulum.29 4) inhibition of Ca++-Mg++-ATPase.46 and 5) reduction of plasma antioxidant capacity and significant increase in circulating free radicals.26

Su &Chen48 showed that methyl mercury promotes a biphasic effect on rat atrial tissue. Initially, when the atrial tissues are exposed to low concentrations (0.5 to 2 ppm) a positive inotropic effect occurs, accompanied by a deficit of contractility as the metal concentration is increased (2 to 50 ppm). These functional findings were accompanied by structural changes in the papillary muscles and atria, as swelling of mitochondria and sarcoplasmic reticulum (SR). Other studies also show how different concentrations of HgCl2 influence the contractile force of papillary muscle and right ventricle strips, alter the kinetics of activatorcalcium; the activity of contractile proteins, the operation of SR.3,9,14,18,39

Moreover, considering that little was known about the effects of the metal on the cardiocirculatory activity we started in our laboratory, since 1991, studies of acute toxic effects of mercury on the cardiovascular system. Until then few studies had shown, as described above, that mercury diminishes myocardial contractility and promoting a drop in blood pressure.43,48 Based on biochemical actions of mercury, inhibition of activity ATPase (Na, K-ATPase and Ca-ATPase) by interacting with the protein SH groups,11,32,39,41,42 data from our laboratory showed that the metal has a similar effect as digitalis at low concentrations (0.5 to 1 uM – positive inotropic effect) followed by depression of contractility at higher concentrations.39,50 These observations are based on the fact that mercury, even at these low concentrations is capable of inhibiting the activity of Na,K-ATPase11 leading to increased intracellular concentration of Na, which in turn reduces the activity of Na/Caexchanger by increasing intracellular Ca.5-7 Ca is then picked up by the sarcoplasmic reticulum, increasing its concentration in this organelle. This effect, although small, is capable during the activation of contraction, to promote small increases in the release of activatorCa by the sarcoplasmic reticulum, generating greater contractile response.

An interesting aspect is that the effects on the increase in developed force were in percentage smaller than the effects on the time derivative of the force. It increased earlier and returned to baseline with a mercury concentration that have depressed the force development.39 As the time derivative is inversely proportional to time we observed that mercury interacts with the ryanodine channel of the sarcoplasmic reticulum and accelerate the release of calcium from the reticulum, which promotes an increase more marked in the time derivative.9,39 Another aspect observed in the slices of right ventricle was that mercury exposure (20 nM) enhanced the effects of positive inotropic interventions, since the metal increased intracellular calcium concentration.

Studies show that in the cardiovascular system mercury causes a decrease in blood pressure and heart rate, increased PR interval of the electrocardiogram, an increased incidence of arrhythmias and atrioventricular conduction block.33 On blood pressure and heart rate of anesthetized rats, mercury administration (5 mg/kgof HgCl2, in rats), promotes a significant drop in blood pressure and heart rate.44 Our results also demonstrated that these effects are accompanied by increased diastolic pressure, both in the left and in the right ventricle, increased right ventricular systolic pressure and the left ventricle systolic pressure reduced. The increase in right ventricular systolic pressure showed a negative linear correlation with the partial pressure of oxygen. Moreover, the reduction of the partial pressure of oxygen promotes pulmonary vasoconstriction, and this finding explains the pulmonary hypertension. However, pulmonary arterial perfusion bed with mercury exposure also showed a significant pulmonary vasoconstriction.44 Thus, two important effects were contributing to the development of pulmonary hypertension, reduction of the partial pressure of oxygen and the vasoconstrictor effect caused by mercury.

We also confirmed that on the heart, both in isolated preparations and in anesthetized rats, the negative inotropic effect was due to inhibition of the myosin ATPase and a calcium overload associated with an increased production of free radicals. However, in anesthetized animals, the drop in blood pressure caused by mercury acute administration is accompanied with a diastolic heart failure and pulmonary hypertension. The latter fact was the result of a potent vasoconstrictor effect of mercury on the pulmonary vessels.

Interestingly, the bradycardia resulting from the acute exposure to mercury is blocked by atropine. At the same time there is a reduction of the hypotensive and of the negative chronotropic response to acetylcholine. This was due to the fact that the acute administration of Hg promotes an increase of plasma and myocardial cholinesterase activity.44

However, the acute exposure to nanomolar mercury concentration increased systolic and diastolic blood pressure, heart rate and blood pressure reactivity to phenylephrine.34 Moreover, Cunha et al.14 showed that the toxic effects of mercury on ventricular contractility is different in the right and left ventricles, as in the first mercury increases contractility fact that contradicts results obtained with left ventricular preparations, from both isolated papillary muscles and with perfused hearts.39,50 Another interesting finding is that acute mercury treatment (20 mM) in the right ventricle slices promotes potentiation of inotropic effects caused by increased extracellular calcium and β-adrenergic stimulation with isoproterenol.18 This effect is supported by the mercury inhibition of the sodium pump, which increases intracellular sodium and reduces the exchanger activity of the Na/Ca exchanger increasing intracellular calcium concentration.

In isolated hearts acutely exposed to 20 mM HgCl2 the metal exposure increases the diastolic pressure of the left ventricle3 and increases dose-dependently (0.1 to 3 mM of HgCl2) this parameter in the right ventricle.14 Mercury also causes a decrease of isovolumic left ventricular systolic pressure immediately after exposure to 0.5, 1, 2and 10 uM after 30 minutes of exposure to 20 nM.3,33 However, the metal exposure does not modify the response of the heart to stretch, ie, those hearts have self-preserved the heterometric regulation mechanism.33

In addition, mercury has direct actions on blood vessels. In our laboratory, studying the tail vascular bed of rats we reported that mercury has vasoconstrictor actions as a result from the reduction of the endothelium-dependent vasodilator activity and the generation of superoxide anions by stimulating the production of vasoconstrictors derived from the cyclooxygenase pathway.15 In rat tail arteries, HgCl2 (6 nM) increased the contractile response to phenylephrine and angiotensin II production by activation of the angiotensin converting enzyme.51

The results described above were obtained with micro and nanomolar mercury concentrations. However, recently, other studies have shown that mercury concentrations in blood and plasma increase after removal of amalgam fillings27,28,31 and, in addition, Salonen et al.45 reported data suggesting a correlation between the consumption of foods with high concentrations of mercury and cardiovascular diseases. Other studies also correlate mercury exposure with increased risk of myocardial infarction and coronary heart disease.23,54 In inhabitants of Amazon, who are exposed to mercury through frequent fish consumption, there was a strong positive correlation between blood concentrations of Hg and arterial blood pressure.19

From 2006, with the aproval of an International Cooperation project from CAPES, with the Universidade Autonoma of Madrid (UAM), Spain, we began studies of chronic actions of mercury at nanomolar concentrations.52 In this study normotensive Wistar rats received for 30 days, low doses of mercury and underwent blood pressure measurements, metabolic control and then vascular reactivity studies with rings of aorta and mesenteric resistance arteries were performed. Some important results have already been obtained and among them we can highlight the following: At the end of treatment the rats exposed to mercury had blood mercury levels of 7.97 ± 0.59 ng/mL, values compatible with those found in exposed individuals.52 We did not observe changes in systolic blood pressure. With regard to cardiac and hemodynamic effects of treatment with mercury, for 30 days we observed that the hemodynamic parameters showed a single change, an increased end diastolic pressure of the left ventricle (LVEDP) in the Mercury group compared to control. However, in isolated hearts from the exposed group to HgCl2 we observed, decrease of developed pressure and time derivatives at baseline conditions and in all diastolic pressures studied. The hearts of the Mercury group also showed a decrease in β-adrenergic response.21,22

However, chronic treatment with HgCl2 was not able to change the contractile parameters in LV papillary muscles but increased the activity of the myosin Ca2+-ATPase and inhibited the specific activity of Na,K-ATPase. Possibly, the increased of LVEDP in vivo and the negative inotropic effect in isolated hearts are due to inhibition of Na,K-ATPase, which causes an increase in intracellular calcium concentration, induce a relaxation defect by calcium overload. Since hemodynamic parameters are preserved in vivo, we can speculate that neurohumoral factors are participating in the maintenance of cardiac inotropism and blood pressure. The increased myosin Ca2+-ATPase activity can also be a compensatory mechanism in heart muscle. We also suggest that the occurrence of a decrease in β-adrenergic response is a result of desensitization of cardiac β receptors by a sympathetic increased activation, as a compensatory mechanism during the exposure to HgCl2.

In summary, on the myocardium and coronary vessels the treatment with mercury for 30 days showed.

1) There is no observed increase in blood pressure.

2) Hemodynamic parameters showed a single change, the increased LV end diastolic pressure.

3) In isolated hearts we observed in the group exposed to HgCl2, reduction of developed pressure and time derivatives at baseline conditions and in almost all studied diastolic pressures, and decreased β-adrenergic response.

4) The treatment was not able to change the contractile parameters in left ventricle papillary muscles but increased the activity of myosin Ca2+-ATPase and inhibited the specific activity of Na,K-ATPase.
5) Coronary endothelial dysfunction by increased production of free radicals.

We can conclude that the exposure to low concentration of HgCl2 promotes negative inotropic effect in isolated hearts, relaxation deficit in vivo, increased myosin ATPase and inhibition of NKA.

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Authors

Dalton Valentim Vassallo1                          

1Doctor in Physiological Sciences – UFRJ, Professor of physiology at UFES/EMESCAM.

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