Isoproterenol potentiation of methyl mercury effectsin vivo on cardiac ATPases and3H-dopamine uptake

Ahammadsahib, K.I.; Moorthy, K.S.; Cameron, J. A.; Desaiah, Durisala

doi:10.1007/bf01881047

Cited by 9 publications

(3 citation statements)

References 14 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In the mM range a dose-dependent reduction of time to peak tension occurs because mercury triggers calcium release from sarcoplasmic reticulum (Abramson and Salama, 1989;Prabhu and Salama, 1990). Since the metal also reduces Ca uptake by inhibiting the 2q sarcoplasmic reticulum Ca -ATPase (Ahammad-2q Sahib et al, 1988;Hechtenberg and Beyersmann, 1991), the release of Ca upon activation reduces 2q post-rest relative potentiation (Oliveira et al, 1994a). Besides, the reduction of tetanic tension development was also observed (Oliveira et al, 1994a;Vassallo et al, 1999).…”

Section: Introductionmentioning

confidence: 97%

Effects of mercury on myosin ATPase in the ventricular myocardium of the rat

Moreira

2003

Comparative Biochemistry and Physiology Part C: Toxicology &

View full text Add to dashboard Cite

Section: Introductionmentioning

confidence: 97%

Effects of mercury on myosin ATPase in the ventricular myocardium of the rat

Moreira

2003

Comparative Biochemistry and Physiology Part C: Toxicology &

View full text Add to dashboard Cite

“…At a biochemical level, mercury is known to interact with SH groups of proteins, altering their activities [5]. Effects that depress ATP hydrolysis and Na + /K + -ATPase activity have been described in nervous tissue and brain microsomes [6][7][8][9][10]. Some epidemiological studies have indeed found an association between increased levels of mercury in the body and a risk of cardiovascular disease [11][12][13].…”

Section: Introductionmentioning

confidence: 99%

Chronic HgCl2 treatment increases vasoconstriction induced by electrical field stimulation: role of adrenergic and nitrergic innervation

et al. 2011

View full text Add to dashboard Cite

In the present study, we have investigated the possible changes in rat mesenteric artery vascular innervation function caused by chronic exposure to low doses of HgCl(2) (mercuric chloride), as well as the mechanisms involved. Rats were divided into two groups: (i) control, and (ii) HgCl(2)-treated rats (30 days; first dose, 4.6 μg/kg of body weight; subsequent dose, 0.07 μg·kg-1 of body weight·day-1, intramuscularly). Vasomotor response to EFS (electrical field stimulation), NA (noradrenaline) and the NO donor DEA-NO (diethylamine NONOate) were studied, nNOS (neuronal NO synthase) and phospho-nNOS protein expression were analysed, and NO, O(2)- (superoxide anion) and NA release were also determined. EFS-induced contraction was higher in the HgCl(2)-treated group. Phentolamine (1 μmol/l) decreased the response to EFS to a greater extent in HgCl(2)-treated rats. HgCl(2) treatment increased vasoconstrictor response to exogenous NA and NA release. L-NAME (N(G)-nitro-L-arginine methyl ester; 0.1 mmol/l) increased the response to EFS in both experimental groups, but the increase was greater in segments from control animals. HgCl(2) treatment decreased NO release and increased O(2)- production. Vasodilator response to DEA-NO was lower in HgCl(2)-treated animals. Tempol increased DEA-NO-induced relaxation to a greater extent in HgCl(2)-treated animals. nNOS expression was similar in arteries from both experimental groups, whereas phospho-nNOS was decreased in segments from HgCl(2)-treated animals. HgCl(2) treatment increased vasoconstrictor response to EFS as a result of, in part, reduced NO bioavailability and increased adrenergic function. These findings offer further evidence that mercury, even at low concentrations, is an environmental risk factor for cardiovascular disease.

show abstract

“…In isolated papillary muscles 1 µM HgCl 2 increases force and rate of force development but above this concentration force is reduced (4,7). These cardiac effects result from a calcium overload developed as a consequence of the reduction of the sarcolemmal Na + ,K + -ATPase (8)(9)(10)(11)(12)(13) and of the sarcoplasmic reticulum (SR) Ca 2+ -ATPase activities (6,9,14,15). Simultaneous effects of Hg 2+ on the Ca 2+ channels of the SR also occur, increasing Ca 2+ release (16,17).…”

Section: Introductionmentioning

confidence: 99%

Effects of mercury on the arterial blood pressure of anesthetized rats

Rossoni

Amaral

Vassallo

et al. 1999

Braz J Med Biol Res

View full text Add to dashboard Cite

The available data suggests that hypotension caused by Hg 2+ administration may be produced by a reduction of cardiac contractility or by cholinergic mechanisms. The hemodynamic effects of an intravenous injection of HgCl 2 (5 mg/kg) were studied in anesthetized rats (N = 12) by monitoring left and right ventricular (LV and RV) systolic and diastolic pressures for 120 min. After HgCl 2 administration the LV systolic pressure decreased only after 40 min (99 ± 3.3 to 85 ± 8.8 mmHg at 80 min). However, RV systolic pressure increased, initially slowly but faster after 30 min (25 ± 1.8 to 42 ± 1.6 mmHg at 80 min). Both right and left diastolic pressures increased after HgCl 2 treatment, suggesting the development of diastolic ventricular dysfunction. Since HgCl 2 could be increasing pulmonary vascular resistance, isolated lungs (N = 10) were perfused for 80 min with Krebs solution (continuous flow of 10 ml/min) containing or not 5 µM HgCl 2 . A continuous increase in pulmonary vascular resistance was observed, suggesting the direct effect of Hg 2+ on the pulmonary vessels (12 ± 0.4 to 29 ± 3.2 mmHg at 30 min). To examine the interactions of Hg 2+ and changes in cholinergic activity we analyzed the effects of acetylcholine (Ach) on mean arterial blood pressure (ABP) in anesthetized rats (N = 9) before and after Hg 2+ treatment (5 mg/kg). Using the same amount and route used to study the hemodynamic effects we also examined the effects of Hg 2+ administration on heart and plasma cholinesterase activity (N = 10). The in vivo hypotensive response to Ach (0.035 to 10.5 µg) was reduced after Hg 2+ treatment. Cholinesterase activity (µM h -1 mg protein -1 ) increased in heart and plasma (32 and 65%, respectively) after Hg 2+ treatment. In conclusion, the reduction in ABP produced by Hg 2+ is not dependent on a putative increase in cholinergic activity. HgCl 2 mainly affects cardiac function. The increased pulmonary vascular resistance and cardiac failure due to diastolic dysfunction of both ventricles are factors that might contribute to the reduction of cardiac output and the fall in arterial pressure. Correspondence

show abstract

Isoproterenol potentiation of methyl mercury effectsin vivo on cardiac ATPases and3H-dopamine uptake

Cited by 9 publications

References 14 publications

Effects of mercury on myosin ATPase in the ventricular myocardium of the rat

Effects of mercury on myosin ATPase in the ventricular myocardium of the rat

Chronic HgCl2 treatment increases vasoconstriction induced by electrical field stimulation: role of adrenergic and nitrergic innervation

Effects of mercury on the arterial blood pressure of anesthetized rats

Contact Info

Product

Resources

About