Cadmium-induced elevation of blood pressure

Nomiyama, Kazuo; Nomiyama, Hiroko

doi:10.1002/(sici)1520-670x(2000)13:1<155::aid-jtra16>3.0.co;2-v

Cited by 7 publications

(1 citation statement)

References 41 publications

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“…The abrupt fall in mean arterial pressure between baseline (week 0) and week 5 may be attributed to the lack of conditioning of the animals to the blood pressure protocol. A review by Nomiyama and Nomiyama (2000) suggests that changes in blood pressure are dependent on the Cd dose such that prolonged exposure of a low dose may elevate blood pressure marginally whereas a higher Cd dose may depress blood pressure, only in hypertensive individuals. This suggests that Cd exposure tends to alter blood pressure in hypertensive animals.…”

Section: Discussionmentioning

confidence: 99%

Cadmium-induced endothelial dysfunction mediated by asymmetric dimethylarginine

Al‐Naemi

Das

2020

Environ Sci Pollut Res

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Cadmium (Cd) is a naturally occurring toxic heavy metal with no known essential biological functions. Exposure to Cd increases the risk of cardiovascular disease by disrupting vascular homeostasis at the endothelium. The aim of the study was to evaluate the effect of chronic low-dose Cd on vascular structure and function. Fifty adult male Sprague Dawley rats were grouped and assigned to one of two treatments for 14 weeks. The control group received normal water for 14 weeks while the Cd-treated group received 15 mg Cd/kg B.W. as CdCl 2 in water for 10 weeks. A subset of the Cd-treated group received 15 mg Cd/kg B.W. as CdCl 2 in water for 10 weeks followed by 4 weeks of normal water. Results show an overall decline in vascular function and structure. Withdrawal of Cd treatment showed a considerable restoration of vascular structure and vasorelaxation function. Additionally, asymmetric dimethylarginine (ADMA) bioavailability was found to be lowered over time. Interestingly, the expression of eNOS in the Cd-treated group was found to be significantly elevated during the exposure by more than 3-fold in comparison with that in the control group. This protein expression was similar to the control group after the withdrawal of Cd treatment. Taken together, the results suggest that ADMA, an eNOS inhibitor, may play a role in altering endothelial function in the presence of cadmium. In conclusion, the findings indicate that even at low doses, Cd leads to endothelial dysfunction mediated by ADMA.

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Section: Discussionmentioning

confidence: 99%

Cadmium-induced endothelial dysfunction mediated by asymmetric dimethylarginine

Al‐Naemi

Das

2020

Environ Sci Pollut Res

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Effects of Acute and Chronic Cadmium Administration on the Vascular Reactivity of Rat Aorta

et al. 2006

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The effect of acute and chronic cadmium (Cd) administration on the vascular function of the rat aorta was studied. The rats were randomly divided into four main groups (A: saline controls under chronic administration, B: Cd-treated rats under chronic administration, C: saline controls under acute administration, D: Cd-treated rats under acute administration). After their sacrifice, the aortic rings were divided into rings with endothelium (E+) and without (E-), and suspended in an isolated organ bath with Krebs - Henseleit buffer. Maximal tension (T max, in g) was measured in response to potassium chloride (KCl) and phenylephrine (PE) in all aortic rings. Relaxation response to acetylcholine (ACh) administration was expressed as percent of maximal tension induced by PE. Chronic administration: A statistically significant increase of the contraction was observed between groups B (i.m. Cd 0.5 mg/kg for 120 days) and A (i.m. 0.9% NaCl for 120 days) in response to KCl (20-60 mM) and the T max as well (in both the E+ and the E- subgroups). No statistically significant difference was observed in response to PE and ACh exposure. Acute administration: A statistically significant increase was observed between group D(E+) (i.m. Cd 2 mg/kg, 8 h before sacrifice) and group C(E+) (i.m. 0.9% NaCl, 8 h before sacrifice) in response to 10-30 mM of KCl, and a significant decrease between D(E-) and C(E-) in response to 10(-7)-10(-6) M of PE, though T (max) was increased between D(E-) and C(E-) with PE exposure. The contractile response levels of the E+ aortic rings to PE and ACh showed no statistically significant difference.

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Evaluation of Toxic Elements in Scalp Hair Samples of Myocardial Infarction Patients at Different Stages as Related to Controls

Afridi

Kazi

et al. 2009

Biol Trace Elem Res

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In the present study, the association of arsenic, cadmium, lead, and nickel between scalp hair samples and mortality from myocardial infarction (MI) patients at first, second, and third heart attack was studied. The biological samples of 130 MI patients (77 male and 53 female) age ranged (45-60 years), were collected and 61 healthy persons of same age group (33 male and 28 female) was selected as control subjects. The toxic elements (TEs) in biological samples were assessed by the electrothermal atomic absorption spectrophotometry prior to microwave-assisted acid digestion. The validity of methodology was checked by the certified human hair reference material (BCR 397). It was observed during the study that 78% of 32 patients of the third MI, age >50 years were expired. In these subjects, the level of As, Cd, Ni, and Pb were increased by 10.6%, 19.5%, 15.7%, and 9.8% in the scalp hair as compared to those who tolerated third MI attack (p = 0.12). The high level of toxic metals may play a role in the development of heart disease in the subjects of this study.

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Cadmium-induced elevation of blood pressure

Cited by 7 publications

References 41 publications

Cadmium-induced endothelial dysfunction mediated by asymmetric dimethylarginine

Cadmium-induced endothelial dysfunction mediated by asymmetric dimethylarginine

Effects of Acute and Chronic Cadmium Administration on the Vascular Reactivity of Rat Aorta

Evaluation of Toxic Elements in Scalp Hair Samples of Myocardial Infarction Patients at Different Stages as Related to Controls

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