The Change of β-Adrenergic System in Lead-Induced Hypertension

Tsao, Der-An; Yu, Hsin‐Su; Cheng, Juei‐Tang; Ho, Chi-Kung; Chang, Huoy-Rou

doi:10.1006/taap.1999.8871

Cited by 68 publications

(54 citation statements)

References 34 publications

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“…These actions also include direct effects on the excitability and contractility of the heart (8,9), vascular actions on the compliance and contractility of smooth muscle (12)(13)(14), and tissue damage by free radicals (15). 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).…”

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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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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“…Lead may cause enhanced sympathetic nerve activity with increases in circulating epinephrine and norepinephrine levels in conjunction with decreased density of vasodilating beta 2 adrenergic receptors [33]. Chronic low-level exposure to lead results in increased activity of angiotensin converting enzyme activity and increases in plasma renin, angiotensin II, and aldosterone levels [34].…”

Section: Discussionmentioning

confidence: 99%

Relationship Between Blood Lead Level and Elevated Blood Pressure in Hypertensive Patients: Implication of Nitric Oxide

Meki¹

2011

TONOJ

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Abstract:The correlation between the blood lead (B-Pb ) levels and the values of blood pressure in hypertensive patients was investigated. Moreover, plasma levels of nitric oxide (NO), total antioxidants (TAOX) and malondialdehyde (MDA) were detected to investigate the correlations between the measured parameters and B-Pb levels in hypertensive patients. Fifty-five hypertensive patients were compared with fifty-three age and sex matched control group. The B-Pb levels were detected by flame atomic absorption spectrometry. The plasma levels of NO, TAOX and MDA were measured by colorimetric methods. In the hypertensive patients, B-Pb levels were significantly higher than controls. Concomitantly, the plasma levels of MDA were significantly increased while the plasma levels of NO and TAOX were significantly reduced in the hypertensive patients in comparison with controls. There were significant positive correlations between B-Pb and each of MDA, systolic and diastolic blood pressure. Conversely, a significant negative correlation was found between BPb and NO. Our study indicated that B-Pb level was associated with elevated blood pressure as well as oxidative stress in hypertensive patients. Moreover, the negative correlation between the B-Pb level and NO level may clarify their implication in cardiovascular disease and hypertension.

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“…Lead exposure in rats is associated with a down regulation of the expression of soluble guanylate cyclase, the enzyme that produces cyclic GMP, which mediates NO-induced vasodilation (Marques et al 2001). Lead-induced hypertension is also associated with abnormalities in the adrenergic system, including increased central sympathetic nervous system activity, elevated plasma norepinephrine, and decreased vascular β-adrenergic receptor density (Carmignani et al 2000;Chang et al 1996;Tsao et al 2000). Chronic lead exposure also activates the renin-angiotensin-aldosterone system, either directly or indirectly, through stimulation of the sympathetic nervous system.…”

Section: Cardiovascular Effectsmentioning

confidence: 99%

Characterizing Golden Eagle Risk to Lead and Anticoagulant Rodenticide Exposure: A Review

Herring

Eagles‐Smith

Buck

2017

Journal of Raptor Research

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The Change of β-Adrenergic System in Lead-Induced Hypertension

Cited by 68 publications

References 34 publications

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

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

Relationship Between Blood Lead Level and Elevated Blood Pressure in Hypertensive Patients: Implication of Nitric Oxide

Characterizing Golden Eagle Risk to Lead and Anticoagulant Rodenticide Exposure: A Review

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