Up-regulation in the expression of renin gene by the influence of aluminium

Ezomo, Ojeiru F.; Matsushima, Fumiko; Meshitsuka, Shunsuke

doi:10.1016/j.jinorgbio.2009.07.018

Cited by 13 publications

(7 citation statements)

References 68 publications

(75 reference statements)

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“…More recently, Al was related to the development of hypertension in experimental animals, these effects were related to an increase in renin expression or erythrocyte membrane impairments after acute or chronic Al administration up to 256 mg/kg (Ezomo et al 2009;Zhang et al 2015). In humans, this possible relationship was also seen, where circulating plasma Al levels were related to arterial hypertension (Granadillo et al 1995).…”

Section: Discussionmentioning

confidence: 99%

“…Animals exposed to up to 256 mg Al/kg bw over 120 days showed an increase of blood pressure and impairments in erythrocyte membranes (Zhang et al 2015). Moreover, a single intraperitoneal injection of Al at 0.5 mg/kg promoted up-regulation of renin expression in rats (Ezomo et al 2009). At the vascular bed, our group has recently reported that an acute exposure to Al was sufficient to promote vascular dysfunction with a reduction of vascular reactivity (Schmidt et al 2016).…”

Section: Introductionmentioning

confidence: 93%

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Aluminum exposure at human dietary levels promotes vascular dysfunction and increases blood pressure in rats: A concerted action of NAD(P)H oxidase and COX-2

et al. 2017

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Aluminum (Al) is a non-essential metal and a significant environmental contaminant and is associated with a number of human diseases including cardiovascular disease. We investigated the effects of Al exposure at doses similar to human dietary levels on the cardiovascular system over a 60day period. Wistar male rats were divided into two major groups and received orally: 1) Low aluminum level - rats were subdivided and treated for 60days as follows: a) Untreated - ultrapure water; b) AlCl at a dose of 8.3mg/kg bw for 60days, representing human Al exposure by diet; and 2) High aluminum level - rats were subdivided and treated for 42days as follows: C) Untreated - ultrapure water; d) AlCl at 100mg/kg bw for 42days, representing a high level of human exposure to Al. Effects on systolic blood pressure (SBP) and vascular function of aortic and mesenteric resistance arteries (MRA) were studied. Endothelium and smooth muscle integrity were evaluated by concentration-response curves to acetylcholine (ACh) and sodium nitroprusside. Vasoconstrictor responses to phenylephrine (Phe) in the presence and absence of endothelium and in the presence of the NOS inhibitor L-NAME, the potassium channels blocker TEA, the NAD(P)H oxidase inhibitor apocynin, superoxide dismutase (SOD), the non-selective COX inhibitor indomethacin and the selective COX-2 inhibitor NS 398 were analyzed. Vascular reactive oxygen species (ROS), lipid peroxidation and total antioxidant capacity, were measured. The mRNA expressions of eNOS, NAD(P)H oxidase 1 and 2, SOD1, COX-2 and thromboxane A2 receptor (TXA-2 R) were also investigated. Al exposure at human dietary levels impaired the cardiovascular system and these effects were almost the same as Al exposure at much higher levels. Al increased SBP, decreased ACh-induced relaxation, increased response to Phe, decreased endothelial modulation of vasoconstrictor responses, the bioavailability of nitric oxide (NO), the involvement of potassium channels on vascular responses, as well as increased ROS production from NAD(P)H oxidase and contractile prostanoids mainly from COX-2 in both aorta and mesenteric arteries. Al exposure increased vascular ROS production and lipid peroxidation as well as altered the antioxidant status in aorta and MRA. Al decreased vascular eNOS and SOD1 mRNA levels and increased the NAD(P)H oxidase 1, COX-2 and TXA-2 R mRNA levels. Our results point to an excess of ROS mainly from NAD(P)H oxidase after Al exposure and the increased vascular prostanoids from COX-2 acting in concert to decrease NO bioavailability, thus inducing vascular dysfunction and increasing blood pressure. Therefore, 60-day chronic exposure to Al, which reflects common human dietary Al intake, appears to pose a risk for the cardiovascular system.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 93%

Aluminum exposure at human dietary levels promotes vascular dysfunction and increases blood pressure in rats: A concerted action of NAD(P)H oxidase and COX-2

et al. 2017

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“…Aldosterone biosynthesis is mainly regulated by the renin-angiotensin system. Moreover, it was shown that Al induces the upregulation in the expression of renin gene [80]. Hypoxia is also a stimulant of renin secretion and renin gene expression [81,82], and Al has been reported to create a hypoxic environment in tissues [83].…”

Section: Discussionmentioning

confidence: 99%

Melatonin Prevents Oxidative Stress in Ovariectomized Rats Treated with Aluminium

Contini

Millen

González

et al. 2011

Biol Trace Elem Res

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This study is designed to determine the simultaneous effect of aluminium (Al) and melatonin (Mel) treatment in intact and ovariectomized (Ovx) female rats on oxidative stress and their inter-organ relationship in the kidney and liver. Al-treated rats received an intra-peritoneal injection of solution of aluminium lactate (0.575 mg Al/100 g of body weight, three times a week), during 12 weeks. Mel groups received intra-peritoneal injections of melatonin at a dose of 10 mg/kg/day, 5 days/week, during 12 weeks. The results of this study showed that Al treatment in female rats modifies homeostasis of glutathione and the antioxidant capacity of the rat liver and kidney. The alteration of glutathione homeostasis and oxidative status was not associated with an increased lipid peroxidation in both organs with the exception of the increase observed in the liver of Ovx rats. Al also induced modifications in the activity of some enzymes related to the glutathione cycle: GSH-Px in the liver and kidney and glutathione reductase only in the kidney. Al exposure decreased CAT activity in both the kidney and liver of intact and Ovx groups. The administration of Mel in the intact and castrated females treated with Al seems to reduce oxidative changes in the liver and kidney of intact and Ovx rats.

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“… 37 – 39 Potentially hazardous elements tend to accumulate for long periods of time in various body systems, including bone, kidneys and liver and have sub-clinical effects in the body. 38 , 40 – 42 …”

Section: Discussionmentioning

confidence: 99%

Addressing the Challenge of Potentially Hazardous Elements in the Reduction of Hypertension, Diabetes and Chronic Kidney Disease in the Caribbean

Fevrier-Paul

Soyibo

Silva

et al. 2021

Journal of Health and Pollution

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Background. Environmental surveys have characterized trace elements such as lead (Pb), cadmium (Cd) and arsenic (As) as potential risk factors for non-communicable diseases. There have been few studies conducted in the Caribbean region to explore, define or clarify such findings locally. Furthermore, local pollution control efforts are often juxtaposed against more seemingly immediate economic concerns in poor communities. Objectives. The present commentary is a call to action for the evaluation of potentially hazardous elements as potential risk indicators and/or factors of common noncommunicable diseases in the Caribbean. Discussion. Findings from Jamaican studies have identified exposure to potentially hazardous elements (PHE) via water, food, and other anthropogenic activities to the detriment of the resident population. Several attempts have been made to abate toxic metal exposure in children with relative success. However, high levels of PHE have been noted in vulnerable populations such as patients with hypertension, diabetes mellitus and chronic kidney disease. Currently, there is low priority towards infrastructure building within the Caribbean region that would promote and sustain long term monitoring and better inform environmental polices impacting chronic diseases. Conclusions. Further investigations are needed to clarify the role that PHE play in increasing the risk or progression of non-communicable diseases, especially in vulnerable groups. Competing Interests. The authors declare no competing financial interests.

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Up-regulation in the expression of renin gene by the influence of aluminium

Cited by 13 publications

References 68 publications

Aluminum exposure at human dietary levels promotes vascular dysfunction and increases blood pressure in rats: A concerted action of NAD(P)H oxidase and COX-2

Aluminum exposure at human dietary levels promotes vascular dysfunction and increases blood pressure in rats: A concerted action of NAD(P)H oxidase and COX-2

Melatonin Prevents Oxidative Stress in Ovariectomized Rats Treated with Aluminium

Addressing the Challenge of Potentially Hazardous Elements in the Reduction of Hypertension, Diabetes and Chronic Kidney Disease in the Caribbean

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