Hypertension induced by methyl mercury in rats

Wakita, Yoshiakira

doi:10.1016/0041-008x(87)90185-2

Cited by 63 publications

(45 citation statements)

References 4 publications

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“…43 In rats exposed to high doses of MeHg chloride, changes in normal heart rate variations were induced, 44 and an increase in systolic blood pressure seen in another study persisted for at least 9 months. 45 A link between brainstem functions and autonomic tone is supported by the associations in the present study between BAEP latencies and HRV parameters, especially the LF results.…”

Section: Discussionsupporting

confidence: 78%

Cardiac autonomic activity in methylmercury neurotoxicity: 14-year follow-up of a Faroese birth cohort

Grandjean

Murata

Budtz‐Jørgensen

et al. 2004

The Journal of Pediatrics

198

131

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Section: Discussionsupporting

confidence: 78%

Cardiac autonomic activity in methylmercury neurotoxicity: 14-year follow-up of a Faroese birth cohort

Grandjean

Murata

Budtz‐Jørgensen

et al. 2004

The Journal of Pediatrics

198

131

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“…However, these substances were not controlled as confounders. From experimental studies, Wakita 28 observed that rats chronically exposed to MeHg developed systemic hypertension that persisted for many months after exposure. Increased BP was also detected in rats exposed to MeHg for 26 days.…”

Section: Discussionmentioning

confidence: 99%

Environmental Mercury Exposure and Blood Pressure Among Nunavik Inuit Adults

2009

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Abstract-Epidemiological evidence suggests a negative impact of methylmercury on the cardiovascular system, but findings regarding the effect on blood pressure (BP) are not consistent. We aimed to study the impact of mercury levels on BP among Nunavik Inuit adults. The health survey Qanuippitaa? was conducted in Nunavik (northern Quebec, Canada), and data were obtained from 732 Inuit Ն18 years of age. Anthropometric blood samples, as well as systolic BP and diastolic BP, were assessed. Pulse pressure (systolic BPϪdiastolic BP) was calculated. Mercury blood concentration was used as a biomarker of recent exposure. Simple relations between mercury and BP parameters were studied by using the Pearson correlation, whereas multiple regressions were performed to control for confounders.

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“…However, the extent of the adverse effects induced by Hg in an organism depends on the form of Hg at the time of exposure, the duration of exposure, and the route of exposure. Exposure to all forms of Hg, at least to some extent, has been shown to cause deleterious effects in the cardiovascular system (Carmignani et al, 1992;Soni et al, 1992;Warkany and Hubbard, 1953;Wakita, 1987), gastrointestinal system (Afonso and deAlvarez, 1960;Bluhm et al, 1992;Lundgren and Swensson, 1949;Murphy et al, 1979), liver (Jaffe et al, 1983;Murphy et al, 1979;Samuels et al, 1982), kidneys (Murphy et al, 1979;Rowens et al, 1991;Samuels et al, 1982;Yasutake et al, 1991), and neurological system (Jaffe et al, 1983;Kutsuna, 1968;Lin and Lim, 1993;Tsubaki and Takahashi, 1986).…”

Section: Mercurymentioning

confidence: 99%

Molecular and ionic mimicry and the transport of toxic metals

Bridges

Zalups

2005

Toxicology and Applied Pharmacology

677

460

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Despite many scientific advances, human exposure to, and intoxication by, toxic metal species continues to occur. Surprisingly, little is understood about the mechanisms by which certain metals and metal-containing species gain entry into target cells. Since there do not appear to be transporters designed specifically for the entry of most toxic metal species into mammalian cells, it has been postulated that some of these metals gain entry into target cells, through the mechanisms of ionic and/or molecular mimicry, at the site of transporters of essential elements and/or molecules. The primary purpose of this review is to discuss the transport of selective toxic metals in target organs and provide evidence supporting a role of ionic and/or molecular mimicry. In the context of this review, molecular mimicry refers to the ability of a metal ion to bond to an endogenous organic molecule to form an organic metal species that acts as a functional or structural mimic of essential molecules at the sites of transporters of those molecules. Ionic mimicry refers to the ability of a cationic form of a toxic metal to mimic an essential element or cationic species of an element at the site of a transporter of that element. Molecular and ionic mimics can also be sub-classified as structural or functional mimics. This review will present the established and putative roles of molecular and ionic mimicry in the transport of mercury, cadmium, lead, arsenic, selenium, and selected oxyanions in target organs and tissues.

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Hypertension induced by methyl mercury in rats

Cited by 63 publications

References 4 publications

Cardiac autonomic activity in methylmercury neurotoxicity: 14-year follow-up of a Faroese birth cohort

Cardiac autonomic activity in methylmercury neurotoxicity: 14-year follow-up of a Faroese birth cohort

Environmental Mercury Exposure and Blood Pressure Among Nunavik Inuit Adults

Molecular and ionic mimicry and the transport of toxic metals

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