Effect of chronic lead exposure on the direct and indirect components of the cardiac response to norepinephrine

Hejtmancik, Milton R.; Williams, Betty J.

doi:10.1016/0041-008x(79)90466-6

Cited by 14 publications

(11 citation statements)

References 19 publications

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“…Atrioventricular node excitability (A-H interval), Q-S intervale and heart rate were not affected significantly by lead treatment. These in vivo effects of lead generally parallel those reported in isolated perfused rat heart studies ( 20000 t susceptibility of the heart to ischemia-and catecholamine-induced arrhythmias (ectopic ventricular extrasystoles) has also been shown to be affected by chronic lead exposure (5,17,41). These effects have been demonstrated both in adult rats exposed to lead as neonates (5) and in adult rats exposed to lead (5 or 25 zg/mL drinking water) since weaning for 12 to 16 months (41).…”

Section: Effects On Cardiac Excitabilitymentioning

confidence: 61%

“…Not surprisingly, the extent of the cardiac and vascular involvement appears to escalate as a direct function of the oral lead dose. In general, administration of lead, most commonly as the acetate salt, to experimental animals has been shown to induce myocarditis (42), degenerative structural and biochemical changes affecting the musculature of the heart and vasculature (35,37,42,43), hypertension (4,6,14,38-40), hypercholesterolemia (6,16,19,20), increased arterial plaque deposition (19,20), electrocardiographic disturbances (38,39), accentuated catecholamine-arrhythmogenicity (5,17,41), altered contractile responsiveness of the myocardium to inotropic stimulation (44), and increased vascular reactivity to cx-adrenergic agonists (5,17,41,44). Although incomplete, recent evidence suggests a role for calcium in the chronic and acute toxicity of lead in the cardiovascular system (6).…”

Section: Cardiac Effects Of Lead In Experimental Animalsmentioning

confidence: 99%

“…The experimental findings that have been reported suggest that lead acts at multiple sites within the cardiovascular system. These findings include direct effects on the excitability and contractilil;y of the heart (8-10), vascular sites of action affecting the compliance and contractility of vascular smooth muscle (11)(12)(13)(14)(15), and possibly sites of action within the central nervous system aflecting blood pressure regulation (16)(17)(18). Although somewhat controversial, there are also indications that chronic lead exposure may affect systemic lipid metabolism.…”

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confidence: 98%

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Cardiovascular Actions of Lead and Relationship to Hypertension: A Review

Kopp¹,

Barron²,

Tow³

1988

Environmental Health Perspectives

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Section: Effects On Cardiac Excitabilitymentioning

confidence: 61%

Section: Cardiac Effects Of Lead In Experimental Animalsmentioning

confidence: 99%

mentioning

confidence: 98%

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Cardiovascular Actions of Lead and Relationship to Hypertension: A Review

Kopp¹,

Barron²,

Tow³

1988

Environmental Health Perspectives

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“…This metal also promotes reductions in vascular β-adrenoceptor density and cAMP levels, factors that contribute to increased blood pressure (16). In addition, harmful effects on other possible sites of action as within the central nervous system might occur affecting blood pressure regulation (17,18). The actions of lead on the endothelium seem to involve the release of vasoactive factors, although the findings obtained to date remain controversial.…”

mentioning

confidence: 99%

Acute lead-induced vasoconstriction in the vascular beds of isolated perfused rat tails is endothelium-dependent

Silveira

Lizardo

Souza

et al. 2010

Braz J Med Biol Res

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Chronic lead exposure induces hypertension in humans and animals, affecting endothelial function. However, studies concerning acute cardiovascular effects are lacking. We investigated the effects of acute administration of a high concentration of lead acetate (100 µΜ) on the pressor response to phenylephrine (PHE) in the tail vascular bed of male Wistar rats. Animals were anesthetized with sodium pentobarbital and heparinized. The tail artery was dissected and cannulated for drug infusion and mean perfusion pressure measurements. Endothelium and vascular smooth muscle relaxation were tested with acetylcholine (5 µg/100 µL) and sodium nitroprusside (0.1 µg/100 µL), respectively, in arteries precontracted with 0.1 µM PHE. Concentrationresponse curves to PHE (0.001-300 µg/100 µL) were constructed before and after perfusion for 1 h with 100 µΜ lead acetate. In the presence of endothelium (E + ), lead acetate increased maximal response (E max ) (control: 364.4 ± 36, Pb 2+ : 480.0 ± 27 mmHg; P < 0.05) and the sensitivity (pD 2 ; control: 1.98 ± 0.07, 2.38 ± 0.14 log mM) to PHE. In the absence of endothelium (E -) lead had no effect but increased baseline perfusion pressure (E + : 79.5 ± 2.4, E -: 118 ± 2.2 mmHg; P < 0.05). To investigate the underlying mechanisms, this protocol was repeated after treatment with 100 µM L-NAME, 10 µM indomethacin and 1 µM tempol in the presence of lead. Lead actions on E max and pD 2 were abolished in the presence of indomethacin, and partially abolished with L-NAME and tempol. Results suggest that acute lead administration affects the endothelium, releasing cyclooxygenasederived vasoconstrictors and involving reactive oxygen species.

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“…Tachycardia, sinus block, nodal rhythm, premature atrial contractions, wandering pacemaker, and other arrhythmias have been reported in children (74). Rat pups and adult rats treated with lead during the first weeks of life have shown increased sensitivity to the arrhythmogenic action of epinephrine (36,37).…”

Section: Metalsmentioning

confidence: 99%