Lead exposure and changes in the renin-angiotensin-aldosterone system in man

Campbell, Brian C.; Modesti, Pietro Amedeo; Scott, JB

doi:10.1016/0378-4274(85)90096-7

Cited by 20 publications

(9 citation statements)

References 23 publications

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“…Previous studies have shown that lead increased the synthesis and/or release of renin from the juxtaglomerular apparatus [15], the production of aldosterone [40] and the activity of plasma ACE [41], [11]. In our study, increased systolic arterial pressure was accompanied by elevation of plasma ACE activity in lead-treated rats; furthermore, there was a significant correlation between systolic arterial blood pressure and ACE activity in the plasma of lead-treated rats.…”

Section: Discussionsupporting

confidence: 70%

Low-Level Lead Exposure Increases Systolic Arterial Pressure and Endothelium-Derived Vasodilator Factors in Rat Aortas

et al. 2011

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Chronic lead exposure induces hypertension and alters endothelial function. However, treatment with low lead concentrations was not yet explored. We analyzed the effects of 7 day exposure to low lead concentrations on endothelium-dependent responses. Wistar rats were treated with lead (1st dose 4 µg/100 g, subsequent dose 0.05 µg/100 g, i.m. to cover daily loss) or vehicle; blood levels attained at the end of treatment were 9.98 µg/dL. Lead treatment had the following effects: increase in systolic blood pressure (SBP); reduction of contractile response to phenylephrine (1 nM–100 µM) of aortic rings; unaffected relaxation induced by acetylcholine (0.1 nM–300 µM) or sodium nitroprusside (0.01 nM–0.3 µM). Endothelium removal, N G-nitro-L-arginine methyl ester (100 µM) and tetraethylammonium (2 mM) increased the response to phenylephrine in treated rats more than in untreated rats. Aminoguanidine (50 µM) increased but losartan (10 µM) and enalapril (10 µM) reduced the response to phenylephrine in treated rats. Lead treatment also increased aortic Na+/K+-ATPase functional activity, plasma angiotensin-converting enzyme (ACE) activity, protein expression of the Na+/K+-ATPase alpha-1 subunit, phosphorylated endothelial nitric oxide synthase (p-eNOS), and inducible nitric oxide synthase (iNOS). Our results suggest that on initial stages of lead exposure, increased SBP is caused by the increase in plasma ACE activity. This effect is accompanied by increased p-eNOS, iNOS protein expression and Na+/K+-ATPase functional activity. These factors might be a compensatory mechanism to the increase in SBP.

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Section: Discussionsupporting

confidence: 70%

Low-Level Lead Exposure Increases Systolic Arterial Pressure and Endothelium-Derived Vasodilator Factors in Rat Aortas

et al. 2011

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“…A recent study of Campbell et al (6) found increased PRA and plasma aldosterone in men with occupational exposure to lead for a relatively short period.…”

mentioning

confidence: 92%

Neurohumoral Blood Pressure Regulation in Lead Exposure

Boscolo¹,

Carmignani²

1988

Environmental Health Perspectives

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JSTOR is a not-for-profit service that helps scholars, researchers, and students discover, use, and build upon a wide range of content in a trusted digital archive. We use information technology and tools to increase productivity and facilitate new forms of scholarship. For more information about JSTOR, please contact support@jstor.org. . The National Institute of Environmental Health Sciences (NIEHS) and Brogan & Partners are collaborating with JSTOR to digitize, preserve and extend access to Environmental Health Perspectives.Previous human studies demonstrated that lead exposure may modify the metabolism of catecholamines and of hormones controlled by the hypothalamo-pituitary axis and may affect the kallikrein-kinin system. Zis paper reports unpublished data on the plasma renin activity of leadexposed workers; these results are in agreement with those of previous human and experimental studies suggesting that the synthesis or release of renin is increased after short and moderate exposure to inorganic lead and reduced whenever the exposure is prolonged.Previous experimental investigations demonstrated that lead may act on the cardiovascular system, with effects on the renin-angiotensin system, on the reactivity to stimulation of peripheral catecholaminergic receptors, on sympathetic and vagal tone, and on reactivity to the stimulation of baroreceptors. lEis paper reports the results of a study on male Sprague-Dawley rats that received 0, 15, 30, and 60 llg/mL of lead in drinking water for 18 months. Blood pressure was increased in the rats receiving 30 and 60 ppm of lead; cardiac inotropism was augmented onb in those receiving the higher dose of the metal, and heart rate was not modified. Cardiovascular responses to agonists indicated that lead exposure affects the renin-angiotensin system and induces sympathetic hyperactivity by acting on central and peripheral sympathetic junctions increasing the responsiveness to stimulation of a2-adrenoreceptors and by increasing the reactivity to stimulation of cardiac and vascular -adrenergic and dopaminergic receptors. The cAMP-dependent availability of Ca2+ for contractile mechanisms of the cardiovascular muscle cells was affected by lead.

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“…1) (99,108). Hypertension may also be lationship between the result of lead-induced changes in the using data obtained vasculature, the renin-angiotensin system tional Health and (109)(110)(111), or in renal ion transport Survey (NHANESprocesses (28 (120,121). A more recent and much less invasive test for evaluation of lead burden involves the quantitation of bone lead with in vivo XRF (122)(123)(124)(125)(126)(127)(128)(129)(130)(131)(132).…”

Section: Lead Nephropathymentioning

confidence: 99%