Plasma renin activity and urinary kallikrein excretion in lead-exposed workers as related to hypertension and nephropathy

Boscolo, P; Galli, G; Iannaccone, A; Martino, Francesco; Porcelli, G; Troncone, L

doi:10.1016/0024-3205(81)90550-6

Cited by 21 publications

(13 citation statements)

References 16 publications

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“…Collectively, these results were interpreted by these authors to indicate that excessive blood lead levels may have caused a generalized desensitization of -adrenergic receptors, which depressed the normal circulatory 92 KOPP, BARRON, AND TOW extent of the cardiac complications that develop in humans in response to chronic and acute lead poisoning (21)(22)(23)(24)(25)(26). Myocarditis (21,22), electrocardiographic abnormalities (16,23,24), altered heart rate activity (16,24), slowed ventricular systole (16,25), hypertension (16,(26)(27)(28)(29), and vascular degeneration (16,22) have all been among the reported cardiovascular aberrations detected in humans chronically and acutely exposed to toxic lead levels (Table 1). Although the threshold blood lead level that triggers cardiac involvement and symptoms of cardiotoxicity has not been determined conclusively, it is apparent that environmental and occupational lead exposures that raise blood lead levels above 100 Rg% and 60 Rg% in adults and children, respectively, are frequently associated with transient as well as permanent cardiac and vascular lesions and functional disturbances (21-29).…”

Section: Those Described By Bertel and Co-workers (26)mentioning

confidence: 94%

Cardiovascular Actions of Lead and Relationship to Hypertension: A Review

Kopp¹,

Barron²,

Tow³

1988

Environmental Health Perspectives

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Section: Those Described By Bertel and Co-workers (26)mentioning

confidence: 94%

Cardiovascular Actions of Lead and Relationship to Hypertension: A Review

Kopp¹,

Barron²,

Tow³

1988

Environmental Health Perspectives

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“…This can be done clinically through provocative chelation of lead, and assessment of subsequent lead excretion in the urine (reviewed by Ibels & Pollock 1986). Observations about coexistent hyper-218 tension in patients being chelated for lead-induced nephritis have often been reported (Boscolo et al 1981Lilis et al 1967;Morgan et al 1966;Morgan 1975;Wedeen et al 1979). There has been some interest in the effect chelation therapy has on improving renal function in patients with chronic· lead-induced nephritis (Lilis et al 1967;Wedeen 1982b;Wedeen et al 1979).…”

Section: Renal Failurementioning

confidence: 99%

Chronic Low-Level Lead Exposure

1987

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Lead is a common element in the earth's crust, serving useful purposes in industry, but serving no purpose in the human body. Increase in blood pressure is an important public health problem with numerous factors contributing to many facets of the disease. The relationship of lead exposure and increased blood pressure has long been considered, but only recently critically investigated. Reports of subtle changes in calcium metabolism and renal function, as well as in vitro studies examining end-arteriolar smooth muscle contractility, link lead exposure and increased blood pressure. This paper critically examines the evidence associating chronic low-level lead exposure and increased blood pressure. The review focuses on epidemiological, clinical, and toxicological data. The epidemiological evidence is consistent with low-level exposure to lead causing an elevation in blood pressure. The strength of that association, and the dose-response characteristics, are less certain. Individual resistance and susceptibility could affect the degree of blood pressure elevation. The results of animal and in vitro studies are consistent with the epidemiological evidence, and suggest biologically plausible mechanisms for the association. The most probable mechanisms are intracellular perturbations in calcium metabolism mediated by direct lead effects at the end-arteriole, and indirect effects via renal dysfunction. Better indices of lead exposure and lead activity are needed to quantify these effects in humans. New and safer methods of chelating lead suggest interesting approaches for studying the relationship between lead and hypertension. This link could have significant implications in determining what constitutes a 'safe' level of environmental lead exposure, and whether a proportion of essential hypertension could be 'cured' by chelation therapy.

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“…exposed men and was low or absent in old, hypertensive and/or nephropathic lead-exposed subjects (4,5). In 22 hospitalized lead-exposed workers, there was a weak but statistically significant correlation between urinary kallikrein activity and plasma renin activity (PRA) (5).…”

mentioning

confidence: 99%

“…In 22 hospitalized lead-exposed workers, there was a weak but statistically significant correlation between urinary kallikrein activity and plasma renin activity (PRA) (5).…”

mentioning

confidence: 99%

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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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Plasma renin activity and urinary kallikrein excretion in lead-exposed workers as related to hypertension and nephropathy

Cited by 21 publications

References 16 publications

Cardiovascular Actions of Lead and Relationship to Hypertension: A Review

Cardiovascular Actions of Lead and Relationship to Hypertension: A Review

Chronic Low-Level Lead Exposure

Neurohumoral Blood Pressure Regulation in Lead Exposure

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