Cadmium as hypertensive agent. Effect on ion excretion in rats

Peña, Alejandro; Iturri, Sergio J.

doi:10.1016/0742-8413(93)90139-c

Cited by 6 publications

(9 citation statements)

References 6 publications

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“…Cd-exposed hypertensive rats showed increased mortality and marked renal vascular changes (Schroeder 1964). In addition, they showed aortic atherosclerosis (Revis et al 1981), increased retention of radioactively labelled sodium administered by intraperitoneal injection (Perry and Erlanger 1981) and reduced urinary volume and sodium excretion (Pena and Iturri 1993). These signs overlap those seen in some forms of human essential hypertension.…”

Section: Nephropathy and Hypertension: Are They Linked ? 21 Expermentioning

confidence: 64%

Kidney Dysfunction and Hypertension: Role for Cadmium, P450 and Heme Oxygenases?

Satarug

Nishijo

Lasker

et al. 2006

Tohoku J. Exp. Med.

103

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Section: Nephropathy and Hypertension: Are They Linked ? 21 Expermentioning

confidence: 64%

Kidney Dysfunction and Hypertension: Role for Cadmium, P450 and Heme Oxygenases?

Satarug

Nishijo

Lasker

et al. 2006

Tohoku J. Exp. Med.

103

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“…The action mechanisms of urban pollutants able to modify BP values are still not clear. In studies on animals 1,2,4,5) and human subjects 2,3) the relationship between cadmium exposure and hypertension has been discussed. Hypertensive response in rats 5) and in male workers exposed to cadmium 3) seems to be timedependent.…”

Section: Discussionmentioning

confidence: 99%

“…Hypertensive response in rats 5) and in male workers exposed to cadmium 3) seems to be timedependent. The hypertension may be due to an accumulation of this metal in the renal parenchyma [1][2][3][4][5] . Studies in the literature have suggested an association between high levels of blood lead and high BP in different categories of workers exposed, such as: police officers 8) , welders and PVC-workers (polyvinyl chloride) 9) , industrial workers and subjects exposed to vehicle smoke 10) , workers in the metal industry or other industrial activities 11) .…”

Section: Discussionmentioning

confidence: 99%

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Ambulatory (24 Hour) Blood Pressure Monitoring in Police Officers

Tomei

Rosati

Baccolo

et al. 2004

Journal of Occupational Health

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Ambulatory (24 Hour) Blood Pressure Monitoring in Police Officers: Francesco Tomei, et al. University of Rome “La Sapienza”, Department of Occupational Medicine, Italy—The aim of the study is to evaluate, by ambulatory (24 h) blood pressure monitoring (ABPM), whether police officers exposed to urban pollutants and possible psycho‐social stressors could be at risk of changes in ambulatory systolic blood pressure (SBP), and ambulatory diastolic blood pressure (DBP) compared to controls. After excluding the principal confounding factors, police officers and controls have been subdivided into non‐smoker and smoker subjects. Police officers were compared by sex, age, length of service, family history of cardiovascular disease, serum total cholesterol, serum HDL cholesterol, serum LDL cholesterol, plasma triglyceride, body mass index (BMI kg/m2) and drinking habits with controls. Smoker police officers were compared with controls also by the smoking habit. In the non smoker group 77 police officers with outdoor activity (38 men and 39 women) and 87 controls with indoor activity (43 men and 44 women) were studied. In the smoker group 43 police officers (21 men and 22 women) and 29 controls (15 men and 14 women) were studied. In non smoker male police officers ambulatory SBP mean values during 24 h, during day‐time and during night‐time were significantly higher than controls. In the same group ambulatory DBP values during 24 h and between 6 AM and 11 AM and between 10 PM and 6 AM were significantly higher in police officers than controls. The results suggest that occupational exposure to urban pollutants and possible psychosocial stressors could cause changes in ABPM values in male police officers compared to controls.

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“…Among the Cd-induced dysfunctions, elevated blood pressure and hypertension have been given special atten tion because of the high incidence in developed indus trialized countries [1,[7][8][9][10][11][12], Despite several attempts, the mechanism by which Cd induces hypertension is not known properly. The results concerning the measurement of hormone levels involved in the regulation of blood pressure failed to explain the mechanism of Cd-induced blood pressure elevation [8,9,11,13].…”

Section: Introductionmentioning

confidence: 99%

Role of Cadmium-Induced Lipid Peroxidation in the Kidney Response to Atrial Natriuretic Hormone

Öner¹,

Şentürk²,

İzgüt-Uysal³

1996

Nephron

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In order to investigate the role of increased lipid peroxidation in the development of cadmium-induced hypertension, 30 male albino rats were exposed to drinking water containing 15 µg/ml cadmium for 30 days, and the results were compared with those of 30 controls. Water containing high cadmium concentrations caused a significant accumulation of the element in blood and kidneys, associated with an obvious elevation in blood pressure. The systolic and diastolic blood pressures rose from 102.8 ± 7.0 and 81.2 ± 3.8 mm Hg to 128.1 ± 4.6 and 107.9 ± 7.4 mm Hg, respectively, in cadmium-treated rats (p < 0.01). A decreased glomerular filtration rate and increased serum creati-nine levels were accompanied by elevated levels of cortical and medullary thiobarbituric acid reactive substances in cadmium-induced hypertensive rats. The mean thiobarbituric acid reactive substance level rose from a control value of 211.5 ± 64.1 to 303.3 ± 46.3 nmol/g protein (p < 0.01) in the renal cortex due to the high intake of cadmium. Despite its obvious diuretic and natriuretic action in control animals, the bolus injection of 1.2 and 2.4 µg/kg atrial natriuretic peptide corrected neither elevated blood pressure nor the reduced glomerular filtration rate in rats exposed to cadmium. However, the tubular response to atrial natriuretic peptide remained unaltered. These data suggest that a lack of vascular response to atrial natriuretic peptide is one of the many putative causes of cadmium-induced hypertension, and cadmium-mediated increased lipid peroxidation may be involved in this unresponsiveness.

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Cadmium as hypertensive agent. Effect on ion excretion in rats

Cited by 6 publications

References 6 publications

Kidney Dysfunction and Hypertension: Role for Cadmium, P450 and Heme Oxygenases?

Kidney Dysfunction and Hypertension: Role for Cadmium, P450 and Heme Oxygenases?

Ambulatory (24 Hour) Blood Pressure Monitoring in Police Officers

Role of Cadmium-Induced Lipid Peroxidation in the Kidney Response to Atrial Natriuretic Hormone

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