Urinary Excretion of Zinc in Patients With Essential Arterial Hypertension

Zozaya, J.L. Garcia; Viloria, M. Padilla; Castro, Albert

doi:10.1016/s0022-5347(17)47605-1

Cited by 6 publications

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“…An association between increases in erythrocyte Zn 2ϩ and essential hypertension has been reported (32). A relationship between urinary Zn 2ϩ excretion and blood pressure has not been established, although studies with small numbers of patients have suggested an association between increases in urinary Zn 2ϩ excretion and hypertension (33,34).…”

Section: External Zn 2ϩ Activates ␣␤␥ Menac Expressed In Xenopusmentioning

confidence: 99%

Extracellular Zn2+ Activates Epithelial Na+ Channels by Eliminating Na+ Self-inhibition

Sheng

Perry

Kleyman

2004

Journal of Biological Chemistry

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Inhibition of epithelial Na ؉ channel (ENaC) activity by high concentrations of extracellular Na ؉ is referred to as Na ؉ self-inhibition. We investigated the effects of external Zn 2؉ on whole cell Na ؉ currents and on the Na ؉ self-inhibition response in Xenopus oocytes expressing mouse ␣␤␥ ENaC. Na ؉ self-inhibition was examined by analyzing inward current decay from a peak current to a steady-state current following a fast switching of a low Na ؉ (1 mM) bath solution to a high Na ؉ (110 mM) solution. Our results indicate that external Zn 2؉ rapidly and reversibly activates ENaC in a dose-dependent manner with an estimated EC 50 of 2 M. External Zn 2؉ in the high Na ؉ bath also prevents or reverses Na ؉ self-inhibition with similar affinity. Zn 2؉ activation is dependent on extracellular Na ؉ concentration and is absent in ENaCs containing ␥H239 mutations that eliminate Na ؉ self-inhibition and in ␣S580C␤␥ following covalent modification by a sulfhydryl-reactive reagent that locks the channels in a fully open state. In contrast, external Ni 2؉ inhibition of ENaC currents appears to be additive to Na ؉ self-inhibition when Ni 2؉ is present in the high Na ؉ bath. Pretreatment of oocytes with Ni 2؉ in a low Na ؉ bath also prevents the current decay following a switch to a high Na ؉ bath but rendered the currents below the control steady-state level measured in the absence of Ni 2؉ pretreatment. Our results suggest that external Zn 2؉ activates ENaC by relieving the channel from Na ؉ self-inhibition, and that external Ni 2؉ mimics or masks Na ؉ self-inhibition.

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Section: External Zn 2ϩ Activates ␣␤␥ Menac Expressed In Xenopusmentioning

confidence: 99%

Extracellular Zn2+ Activates Epithelial Na+ Channels by Eliminating Na+ Self-inhibition

Sheng

Perry

Kleyman

2004

Journal of Biological Chemistry

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Zinc Content in Lymphocytes and the Activity of Zinc Ion Efflux from Lymphocytes in Primary Arterial Hypertension

Tubek¹

2005

BTER

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Clinical observations and experimental data show that zinc (Zn) plays a role in regulating arterial blood pressure and in arterial hypertension etiopathogenesis. To determine the direction of changes in Zn metabolism in primary arterial hypertension, Zn absorption from the alimentary tract, Zn levels in blood serum, its content in lymphocytes, Zn efflux rate constants from lymphocytes, and urinary Zn excretion in patients with hypertension and in healthy subjects were studied. In this article, Zn levels in blood serum, its content in lymphocytes, and Zn efflux rate constants from lymphocytes are presented. In primary arterial hypertension, on the basis of this study, decreasing Zn levels in blood serum and its decreasing content in lymphocytes were found. The Zn efflux rate constants from lymphocytes increased at the initial stage of hypertension (mild arterial hypertension) and decreased in the late stage of the hypertension disease (severe arterial hypertension). Taking into consideration all of the directions of changes and the fact that Zn can be a factor that increases arterial blood pressure, the changes in Zn distribution can be regarded as having, to a certain extent, a protective character leading to weakening of the pressor reaction, assuming a genetic existence of relative or absolute Zn excess in the body. The changes of Zn distribution can lead, after some time, to Zn deficiency and the resulting metabolic changes (e.g., carbohydrate intolerance).

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Urinary Zinc Excretion Is Normalized in Primary Arterial Hypertension After Perindopril Treatment

Tubek

2006

BTER

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Increased or unchanged urinary zinc excretion has been reported in hypertension. In the present article, this observation was confirmed in a group of 10 untreated hypertensive patients of both sexes that had no diabetes or obesity. The 24-h zinc excretion was significantly different between the patients: 7.46+/-3.01 micromol and healthy controls: 5.19+/-2.19 micromol (p<0.025). After a 1-mo treatment with 4 mg perindopril per day, a decrease of urinary zinc was observed until it reached levels not significantly different from those of the healthy controls (5.98 +/- 2.13 micromol). The decrease was significantly different from that of the pretreatment values (p<0.05).

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Urinary Excretion of Zinc in Patients With Essential Arterial Hypertension

Cited by 6 publications

References 0 publications

Extracellular Zn2+ Activates Epithelial Na+ Channels by Eliminating Na+ Self-inhibition

Extracellular Zn2+ Activates Epithelial Na+ Channels by Eliminating Na+ Self-inhibition

Zinc Content in Lymphocytes and the Activity of Zinc Ion Efflux from Lymphocytes in Primary Arterial Hypertension

Urinary Zinc Excretion Is Normalized in Primary Arterial Hypertension After Perindopril Treatment

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