Alteration of atrial natriuretic peptide levels by short term cadmium treatment

Giridhar, Jaisri; Isom, Gary E.

doi:10.1016/0300-483x(91)90045-3

Cited by 9 publications

(4 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It is also known that Cd induces testicular hypoplasia and inhibits spermatogenesis when fed or injected. Cadmium affects the activity of several important enzymes (Giridhar and Isom, 1991).…”

Section: Tissue Damagementioning

confidence: 99%

Cadmium distribution and toxicity in tissues of small rodents

Świergosz-Kowalewska

2001

Microscopy Res & Technique

110

View full text Add to dashboard Cite

The aim of the present paper is to discuss the accumulation and distribution of cadmium (Cd) in the various tissues of animals, the interactions of cadmium with other elements, and the damage to tissues caused by this metal. Cadmium is not physiologically or biochemically essential to an organism. It is absorbed via the gastrointestinal tract and lungs and accumulated in various tissues, mainly the kidneys and liver. The distribution of cadmium between various tissues depends on many endogenous and exogenous factors. Cadmium is bound to a low-molecular-weight protein, metallothionein (MT), and to high-molecular-weight proteins. This metal has a great affinity to thiol groups. Cadmium binds also to O- and N-containing ligands. The distribution of cadmium between organs differs markedly depending on the chemical form of administered Cd and the duration of exposure. Acute exposure results in a different distribution pattern throughout the body than does chronic exposure. Long-term exposure to high doses of cadmium may cause biochemical and functional changes in some critical organs. Cadmium can influence the absorption and distribution of essential elements and can replace them in enzymes. Metallothionein and glutathione play important roles in the transport of metals and in detoxification processes. Reported findings are mainly the results of experiments on laboratory animals. The lack of data concerning the localization of cadmium in various tissues of wild species is noticeable and there is a great need for such data.

show abstract

Section: Tissue Damagementioning

confidence: 99%

Cadmium distribution and toxicity in tissues of small rodents

Świergosz-Kowalewska

2001

Microscopy Res & Technique

110

View full text Add to dashboard Cite

show abstract

“…Microscopic changes in the aortae of horses living in the soft-water areas showed an association with arteriosclerotic changes and Cd accumulation [32], Nevertheless, there are con flicting results concerning the reasons of Cd-induced hy pertension [8][9][10][11][12][13]. According to Pena and Iturri [12], Cdinduced reduced Na excretion is responsible for the ele vated blood pressure.…”

Section: Discussionmentioning

confidence: 99%

“…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]. Among many explanatory attempts, the results of Giridhar et al [10] who showed a substantial reduction in both density and affinity of receptors for atrial natriuretic peptide (ANP) in Cd-exposed cells are very important to clarify the devel opment of Cd-induced hypertension.…”

Section: Introductionmentioning

confidence: 99%

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

Öner¹,

Şentürk²,

İzgüt-Uysal³

1996

Nephron

View full text Add to dashboard Cite

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.

show abstract

“…A meta-analysis study of published literature found a positive association between hypertension and Cd levels in blood and hair [ 139 ]. Indeed, Cd has been shown to decrease plasma levels of atrial natriuretic peptide (ANP) [ 140 ], an important regulator of blood pressure. Cd appears to reduce the affinity of the ANP receptor for ANP and also decreased the number of binding sites available [ 141 ].…”

Section: Molecular Effects Of Environmental Toxicants On Ckd Progressionmentioning

confidence: 99%

Molecular Mechanisms of Cellular Injury and Role of Toxic Heavy Metals in Chronic Kidney Disease

Mishra

Nichols

Dave

et al. 2022

IJMS

View full text Add to dashboard Cite

Chronic kidney disease (CKD) is a progressive disease that affects millions of adults every year. Major risk factors include diabetes, hypertension, and obesity, which affect millions of adults worldwide. CKD is characterized by cellular injury followed by permanent loss of functional nephrons. As injured cells die and nephrons become sclerotic, remaining healthy nephrons attempt to compensate by undergoing various structural, molecular, and functional changes. While these changes are designed to maintain appropriate renal function, they may lead to additional cellular injury and progression of disease. As CKD progresses and filtration decreases, the ability to eliminate metabolic wastes and environmental toxicants declines. The inability to eliminate environmental toxicants such as arsenic, cadmium, and mercury may contribute to cellular injury and enhance the progression of CKD. The present review describes major molecular alterations that contribute to the pathogenesis of CKD and the effects of arsenic, cadmium, and mercury on the progression of CKD.

show abstract

Alteration of atrial natriuretic peptide levels by short term cadmium treatment

Cited by 9 publications

References 27 publications

Cadmium distribution and toxicity in tissues of small rodents

Cadmium distribution and toxicity in tissues of small rodents

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

Molecular Mechanisms of Cellular Injury and Role of Toxic Heavy Metals in Chronic Kidney Disease

Contact Info

Product

Resources

About