Morphological and functional characteristics of cadmium-induced arterial hypertension

Mikhaleva, L.M.; Zhavoronkov, Alex; Chernyaev, A. L.; Koshelev, V. B.

doi:10.1007/bf00841499

Cited by 7 publications

(10 citation statements)

References 5 publications

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“…Giridhar et al [10] and others [18.34] indicated that Cd-mediated changes in ANP receptor density and affinity may have a causal role in the development of hypertension. Indeed, a lack of vascular response to ANP injection in the present study is in agreement with a decreased receptor affinity as well as with the results of Mikhaleva et al [8] who noted an elevated vascular resistance despite an increased ANP level in Cd-treated rats. The mechanism by which Cd causes an increase in the vascular resistance as reported by Mikhaleva et al [8] or a decrease in receptor affinity to vasodilator hormones such as ANP [10] is not reliably known, but can be attributed to a Cd-induced peroxidative damage of the cell membrane [18][19][20][21], The role of a peroxidative damage in the impaired cell response to hor mones has not been previously studied in Cd-mediated hypertension.…”

Section: Discussionsupporting

confidence: 82%

“…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%

“…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%

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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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Section: Discussionsupporting

confidence: 82%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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

Öner¹,

Şentürk²,

İzgüt-Uysal³

1996

Nephron

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“…This was examined by blocking the α 1 AR with its antagonist prazosin. The Along with these findings, Mikhaleva et al (1991) found that chronic Cd exposure in rats causes hypertrophic effects in the arterial wall as well as the left ventricular cardiomycetes (86). From the viability test, Cd didn't show any signs of cell proliferation, which result in hyperplasia.…”

Section: Controlmentioning

confidence: 88%

Cadmium Modulates Expression Of Vascular Alpha Adrenoceptors And Aortic Smooth Muscle Cells Phenotype

Aboujassoum

2013

Qatar Foundation Annual Research Forum Volume 2013 Issue 1

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Effect of boron on the ultrastructure of parathyrocytes and atrial cardiomyocytes

1997

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Ultrastructural shifts in parathyrocytes and atrial cardiomyocytes induced by long-term treatment with boron-containing water (250 mg/liter) were found against the background of boron accumulation. These changes are indicative of enhanced secretory activity of these cells. It is hypothesized that boron modulates the effect of parathyroid hormone and atrial natriuretic factor and the rate calcium-sodium exchange. Key Words: boron; parathyrocytes; atrial cardiomyocytes; ultrastructural changesPublished data and our previous studies have demonstrated that boron affects the structure of cell membranes [6] and calcium and magnesium metabolism [15], enhances diuresis [121, and reduces blood pressure [1]. It can be hypothesized that boron affects the functioning of the parathyroid gland and production of parathyroid hormone (PTH) which regulates blood calcium level and reduces blood pressure [4]. Moreover, one can expect structural and functional shifts in atrial cardiomyocytes, since atrial natriuretic factor (ANF) is involved into regulation of sodium-calcium exchange and exerts a pronounced antipressor effect [10].There are no published data on the effect of boron on the ultrastructure of parathyrocytes and atrial cardiomyocytes, therefore, these questions were the focus of our investigation. MATERIALS AND METHODSExperiments were carried out on 20 male albino rats weighing 220-250 g. The animals were given sodium tetraborate dissolved in water (250 mg/liter in a volume of 3 ml, pH 8.0, per os). This concentration naturally occurs in mineral water used for the treatment and rehabilitation. Daily dose of boron was Laboratory-of Morphology, Russian Center of Rehabilitation and Physiotherapy, Ministry of Health of the Russian Federation, Moscow 3.75 mg/kg. Control animals received tap water. The total course consisted of 24 procedures. The animals were decapitated after 15 or 24 procedures, and the boron content in the thyroid-parathyroid complex (the parathyroid glands in rats are submerged into the thyroid tissue) and in the heart was determined spectrophotometrically using H-resorcin [9]. Electron microscopy of the parathyroid gland and left atrium was performed after 15 procedures (the maximum tissue accumulation of boron). To this end, specimens were fixed in 2.5% glutaraldehyde and postfLxed with OsO4, dehydrated in alcohol of ascending concentrations and acetone, and embedded in EponAmldite. Ultrathin sections were examined under JEM-100C and JEM-100CX electron microscopes. Quantitative parameters of parathyrocytes and atrial cardiomyocytes were analyzed stereologically and by automorphometry with an MOP-Videoplan device. The volume portion and number of mitochondria, volume portion of granular endoplasmic reticulum (GER), Golgi apparatus, and the area of secretory granules in atrial cardiomyocytes were calculated. RESULTSMaximum accumulation of boron was noted after 15 procedures: its concentration in the thyroid-parathyroid complex and heart increased 3.4-fold (p< 0.05) and 8-fold (p<0.001), respectively (Table ...

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Morphological and functional characteristics of cadmium-induced arterial hypertension

Cited by 7 publications

References 5 publications

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

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

Cadmium Modulates Expression Of Vascular Alpha Adrenoceptors And Aortic Smooth Muscle Cells Phenotype

Effect of boron on the ultrastructure of parathyrocytes and atrial cardiomyocytes

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