Kininergic system and arterial hypertension following chronic exposure to inorganic lead

Carmignani, M.; Boscolo, P; Poma, Anna; Volpe, Anna

doi:10.1016/s0162-3109(99)00115-0

Cited by 79 publications

(71 citation statements)

References 21 publications

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“…A hypertensive effect was also reported and the action of lead is related to impairment of endothelial function and also to the production of free radicals (4,13,26). An increased production of angiotensin II has also been reported as a mechanism to induce hypertension (15).…”

Section: Discussionmentioning

confidence: 99%

“…Few reports show that chronic lead administration acts on the heart enhancing contractility probably by increasing the production of angiotensin II (15). Although chronic treatment increases contractility, acute treatment blocks calcium channels in cardiac myocytes and Xenopus laevis oocytes (18).…”

Section: Discussionmentioning

confidence: 99%

“…The participation of free radicals reducing nitric oxide bioavailability (12) and depletion of antioxidant reserves (4) or its upregulation (13) has been reported. Lead-induced hypertension also involves the participation of peripheral or central nervous system mechanisms, such as the increase of sympathetic nerve activity, reduction of the baroreflex sensitivity and reduction of parasympathetic tone (14,15).…”

Section: Introductionmentioning

confidence: 99%

“…Carmignani et al (11,15) reported increased myocardial inotropism and increased activity of the angiotensin-converting enzyme in rats exposed to 60 ppm lead acetate for 10 months. On the other hand, Williams et al (16) reported negative inotropic effects on perfused hearts caused by acute lead administration.…”

Section: Introductionmentioning

confidence: 99%

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Lead reduces tension development and the myosin ATPase activity of the rat right ventricular myocardium

Vassallo

Lebarch

Moreira

et al. 2008

Braz J Med Biol Res

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Lead (Pb 2+ ) poisoning causes hypertension, but little is known regarding its acute effects on cardiac contractility. To evaluate these effects, force was measured in right ventricular strips that were contracting isometrically in 45 male Wistar rats (250-300 g) before and after the addition of increasing concentrations of lead acetate (3,7,10,30, 70, 100, and 300 µM) to the bath. Changes in rate of stimulation (0.1-1.5 Hz), relative potentiation after pauses of 15, 30, and 60 s, effect of Ca 2+ concentration (0.62, 1.25, and 2.5 mM), and the effect of isoproterenol (20 ng/mL) were determined before and after the addition of 100 µM Pb 2+ . Effects on contractile proteins were evaluated after caffeine treatment using tetanic stimulation (10 Hz) and measuring the activity of the myosin ATPase. Pb 2+ produced concentration-dependent force reduction, significant at concentrations greater than 30 µM. The force developed in response to increasing rates of stimulation became smaller at 0.5 and 0.8 Hz. Relative potentiation increased after 100 µM Pb 2+ treatment. Extracellular Ca 2+ increment and isoproterenol administration increased force development but after 100 µM Pb 2+ treatment the force was significantly reduced suggesting an effect of the metal on the sarcolemmal Ca 2+ influx. Concentration of 100 µM Pb 2+ also reduced the peak and plateau force of tetanic contractions and reduced the activity of the myosin ATPase. Results showed that acute Pb 2+ administration, although not affecting the sarcoplasmic reticulum activity, produces a concentration-dependent negative inotropic effect and reduces myosin ATPase activity. Results suggest that acute lead administration reduced myocardial contractility by reducing sarcolemmal calcium influx and the myosin ATPase activity. These results also suggest that lead exposure is hazardous and has toxicological consequences affecting cardiac muscle.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Lead reduces tension development and the myosin ATPase activity of the rat right ventricular myocardium

Vassallo

Lebarch

Moreira

et al. 2008

Braz J Med Biol Res

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“…Human beings usually have lead in their organism (8) which, upon sufficient exposure and/or accumulation in the body (32,33), can exert adverse effects. Although having no physiological function, its toxic effects on humans and animals have long been known, affecting almost all organs and systems in the human body.…”

Section: Leadmentioning

confidence: 99%

Toxic effects of mercury, lead and gadolinium on vascular reactivity

Vassallo

Simões

Furieri

et al. 2011

Braz J Med Biol Res

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Heavy metals have been used in a wide variety of human activities that have significantly increased both professional and environmental exposure. Unfortunately, disasters have highlighted the toxic effects of metals on different organs and systems. Over the last 50 years, the adverse effects of chronic lead, mercury and gadolinium exposure have been underscored. Mercury and lead induce hypertension in humans and animals, affecting endothelial function in addition to their other effects. Increased cardiovascular risk after exposure to metals has been reported, but the underlying mechanisms, mainly for short periods of time and at low concentrations, have not been well explored. The presence of other metals such as gadolinium has raised concerns about contrast-induced nephropathy and, interestingly, despite this negative action, gadolinium has not been defined as a toxic agent. The main actions of these metals, demonstrated in animal and human studies, are an increase of free radical production and oxidative stress and stimulation of angiotensin I-converting enzyme activity, among others. Increased vascular reactivity, highlighted in the present review, resulting from these actions might be an important mechanism underlying increased cardiovascular risk. Finally, the results described in this review suggest that mercury, lead and gadolinium, even at low doses or concentrations, affect vascular reactivity. Acting via the endothelium, by continuous exposure followed by their absorption, they can increase the production of free radicals and of angiotensin II, representing a hazard for cardiovascular function. In addition, the actual reference values, considered to pose no risk, need to be reducedResearch supported by CAPES and CNPq/FAPES/ FUNCITEC (#39767531/07), Brazil, and MCINN (#SAF 2009-07201) and ISCIII (Red RECAVA, #RD06/0014/0011), Spai

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Lead

Jacobs

2023

Patty's Toxicology

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Lead is an important industrial commodity that has numerous adverse health effects, even at relatively low levels of exposure. The mining of lead‐containing ores began in antiquity and was used in coins, weights, ornaments, cosmetics, utensils, ceramic glazes, solder, paints, gasoline, conduits for drinking water, and others. Although descriptions of the toxic effects of lead appeared very early in history, the association between the use of lead in industry, construction, and commerce and health effects was very slow to evolve. Insights into mechanisms of lead toxicity did not appear until the twentieth century. The correlation between pathological and clinical and sub‐clinical effects of lead on organ systems and routes of exposure in both the workplace and the community are reviewed. There continues to be an extensive body of new scientific literature to this day regarding the effects of lead, which allows for more precise interpretation of relationships between exposure and effect, especially “low level” lead exposures in both children and adults. The best treatment is the prevention of exposure. The objective of this chapter is to integrate the emerging scientific advances in the toxicology of lead with the occurrence and recognition of both clinical and more subtle subclinical effects. A list of current publications regarding health criteria and protective regulatory and guidance measures for exposure to lead in both the occupational setting and the community (with a focus on children) are provided.

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Kininergic system and arterial hypertension following chronic exposure to inorganic lead

Cited by 79 publications

References 21 publications

Lead reduces tension development and the myosin ATPase activity of the rat right ventricular myocardium

Lead reduces tension development and the myosin ATPase activity of the rat right ventricular myocardium

Toxic effects of mercury, lead and gadolinium on vascular reactivity

Lead

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