alexa Magnesium Metabolism, Vitamin D and Interleukins in Cardiovascular Disease | OMICS International
ISSN: 2153-0769
Metabolomics:Open Access
Like us on:
Make the best use of Scientific Research and information from our 700+ peer reviewed, Open Access Journals that operates with the help of 50,000+ Editorial Board Members and esteemed reviewers and 1000+ Scientific associations in Medical, Clinical, Pharmaceutical, Engineering, Technology and Management Fields.
Meet Inspiring Speakers and Experts at our 3000+ Global Conferenceseries Events with over 600+ Conferences, 1200+ Symposiums and 1200+ Workshops on
Medical, Pharma, Engineering, Science, Technology and Business

Magnesium Metabolism, Vitamin D and Interleukins in Cardiovascular Disease

Kisters K1*, Gremmler B2, Gröber U3 and Tokmak F1*

1Med Clinic I, St. Anna Hospital, Hospitalstr. 19, Herne 44649, Germany

2Department of Cardiology, Bottrop, Germany

3Academy for Micronutrients, Essen, Germany

*Corresponding Author:
Kisters K
Med Clinic I, St. Anna Hospital
Hospitalstr. 19, Herne 44649, Germany
Tel: 4923259862100
E-mail: [email protected]

Received Date: May 18, 2016; Accepted Date: June 16, 2016; Published Date: June 20, 2016

Citation: Kisters K, Gremmler B, Gröber U, Tokmak F (2016) Magnesium Metabolism, Vitamin D and Interleukins in Cardiovascular Disease. Metabolomics 6:177. doi:10.4172/2153-0769.1000177

Copyright: © 2016 Kisters K, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Visit for more related articles at Metabolomics:Open Access

Abstract

A magnesium deficiency is known to be involved in the pathogenesis of cardiovascular diseases. In patients with essential hypertension intima media thickness is increased in about 70% (ELSA Study). In our study, we investigated 21 patients (10 female, 11 male, average age 56.3 ± 6.6 years) with untreated essential hypertension (grades I and II according to WHO guidelines). All patients had a hypomagnesiaemia in serum (1.57 ± 0.11 mg%). In all patients we found a significant increase in intima media thickness of arteria carotis communis (0.97 ± 0.08 mm) (r=-0.869, p<0.0001). The results show that a magnesium deficiency in patients with essential hypertension may be of special pathogenetic importance. In addition, the role of magnesium deficiency in the development of arteriosclerosis has to be discussed. Furthermore, we demonstrated a connection between magnesium deficiency and an increased intima media thickness. In this context, calcium antagonist therapy or magnesium supplementation may be of advantage when treating intima media thickness in hypertension. In addition in essential hypertensives with diabetes mellitus type IIb showing lowered magnesium (1.72 ± 0.08 mg/ dl) and vitamin D (9.55 ± 4.74 ng/ml) levels interleukine 6 concentrations were 8.57 ± 4.14 pg/ml (p<0.01 vs. controls) being a risk factor for metabolic disorder, e. g. arteriosclerosis.

Keywords

Magnesium; Cardiovascular disease; Metabolism; Arteriosclerosis; Vitamin D

Introduction

Cardiovascular epidemiology has expanded from studies focusing only on cardiovascular risk factors to include research on causes and consequences of atherosclerosis and associated arterial wall abnormalities. In a large number of studies, techniques have been used that enable non-invasive assessment of vascular characteristics to study early functional and structural wall changes. Examples of these measurements are coronary artery calcium levels, arterial stiffness, brachial endothelial function, aortic augmentation index (Aix) and carotid intima-media thickness (CIMT). One of the reasons for an increased attention on these indicators is that the availability of adequate noninvasively assessed measurements of functional and structural arterial characteristics allows for studies among children, adolescents and young adults. Such studies may greatly enhance our insight in causes, development and pathophysiological mechanisms of cardiovascular disease. Furthermore, these measurement extend research into middle aged and elderly subjects who are yet free from symptomatic cardiovascular disease [1].

Several new studies have focused on the role of CIMT in predicting future vascular events [1,2].

Studies performed in the general population consistently showed a gradual graded increase in risk with increased CIMT. The magnitude of association differed somewhat by age but in general was remarkably similar across studies.

CIMT may help, in addition to established risk factors, in identifying those individuals that will suffer from cerebrovascular and coronary heart disease [3-5].

In this context changes in magnesium metabolism have been implicated in the pathogenesis of hypertension [6-28]. Therefore it was of interest to study magnesium deficient patients with essential hypertension concerning CIMT and arteriosclerosis and vitamin D disorder.

Subjects and Methods

Subjects

21 patients were studied, 11 male and 10 female. The average age was 56.3 ± 6.6 years. All patients had a normal renal function (serumcreatinine 0.85 ± 0.4 mg%). In all patients cholesterol and triglyceride concentrations were significantly increased.

In a second additional study 11 different hypertensive patients with diabetes mellitus type IIb with magnesium loss and lowered vitamin D status were investigated concerning interleukine 6 levels.

All patients were informed about the aim of the study according to the Helsinki Charter and had given written consent at the time of investigation.

Methods

The analysis of serum magnesium concentrations was performed by a Hitachi analyser. Measurements of intima media thickness were performed in the arteria carotis communis with a GE apparatus Vivid 5, Solingen, Germany.

Vitamin D and interleukine 6 measurements were performed in serum by a Hitachi analyser, too.

Statistical Analysis

Statistical analyses was performed using ANOVA.

The results are given as means ± SD, a p<0.05 was considered significant. The reported p values are two-tailed.

Results

The mean serum magnesium concentration was 1.57 ± 0.11 mg/dl (normal range for serum magnesium: 1.70-2.55 mg/dl). IMT (in mm) was measured 0.97 ± 0.8. The normal range is known to be below 0.7 mm. The correlation coefficient r=-0.869, p<0.0001.

In hypertensive diabetics type II serum magnesium levels were 1.72 ± 0.08 mg/dl, which was in the lower normal range or below. Interleukine 6 concentrations were 8.57 ± 4.14 pg/ml, being significantly increased as compared to controls (p<0.01).

Vitamin D levels were significantly decreased in patients with 9.55 ± 4.74 ng/ml (p<0.01) (normal range: >20 ng/ml).

The vitamin D/magnesium ratio was 5.59 ± 2.87 in 11 hypertensive diabetics type IIb, being lower than values of normal range.

Discussion

A role for lowered magnesium concentrations in vascular tone has been postulated in essential hypertension [6-28].

In essential hypertensives, Resnick et al. [29,30] found decreased intracellular free Mg++ concentrations in red blood cells as estimated by nuclear magnetic resonance spectroscopy (29, 30). Analogous findings were reported in red blood cells from spontaneously hypertensive rats [11-16,31].

On the basis of experimental data, the theoretical mechanisms underlying the Mg++-induced vasodilation may be: (a) a modification of the response to vasopressor hormones, and (b) an interaction with cellular Ca++ handling [32]. These possible mechanisms are supported by 3 lines of recent evidence. First, the extracellular Mg++ concentration can influence Ca++ metabolism of vascular smooth muscle by changing the Ca++ influx through the plasma membrane. Recently, in single myocytes from frog ventricle, the site of interaction between Mg++ and Ca++ inward current that is dependent on phosphorylation by cyclic adenosine monophosphatase [33]. Second. Changes in the extracellular Mg++ concentration induced inverse changes in the Ca++ content of vascular smooth muscle and in exchangeable Ca++ [34,35]. Third, a decrease in the intracellular free Mg++ concentration results in diminished membrane Na+, K+-adenosine triphosphatase and Ca++ ATPase activities, and, as a corollary, increased Na+-Ca++ exchange and increased intracellular Na+ and Ca++ concentrations [36]. In addition a sodium magnesium antiport exists in red blood cells and in vascular smooth muscle cells [9]. TRPM (transient receptor potential channel melastin member) type 6 and 7 -channels, recently described, regulate intracellular magnesium stores, too [37,38].

It is well known, that an increased intima media thickness is a marker for cardiovascular morbidity and mortality. Functional and structural arterial measurements confer an increased risk for cardiovascular disease. It has been suggested that the increase in the stiffness of the arterial wall with aging can be explained by a decrease in elastin density (or collagen) [39-45].

Calcification of arteries is a common phenomenon especially in the elderly [34].

Aortic wall calcium (and phosphorus) contents increase with age. Age linked medial calcification is associated with elastic fibers [34]. Physical factors such as increased intraluminal pressure (e.g. hypertension) that promote elastocalcionis suggested that global degeneration of the arterial wall, of stress on medial elastic fibers and lamellae are followed by fracture. As pulse pressure increases in hypertension (especially so in isolated systolic hypertension), cyclic wall stress is increased and so fracture and elastocalcinosis would be expected to occur earlier. In this context it is well documented that magnesium acts as a physiological calcium antagonist and is necessary for an intact phosphorus metabolism. As described early by our group a magnesium deficiency is involved in the pathogenesis of primary hypertension, the development of elevated pulse pressure values and as shown here in an increased intima media thickening [41,43].

In addition a negative correlation concerning magnesium loss and elevated blood lipid composition was described earlier, even by our group.

It is also of recent interest that antihypertensive drug treatment with calcium antagonist is of special benefit in avoiding intima media thickening and thereby in preventing stroke. Calcium antagonists lower blood pressure and reduce cardiovascular morbidity and mortality [44-49].

In addition data presented here show decreased magnesium concentrations and vitamin D levels and increased interleukin levels in hypertensive patients with diabetes mellitus type IIb.

IL-6 plays an important role in the development of arterial stiffness and arteriosclerosis in hypertensive patients and in diabetics. The combination of both hypertension and diabetes shows even more arteriosclerotic organe damage in which IL-6 is pathophysiologically involved [28].

These findings favour the development of an increased intima media thickness and the manifestation of arteriosclerosis.

In conclusion, a vitamin D loss in hypertensive patients with diabetes mellitus type IIb has to be corrected immediately. Normally, the daily amount of magnesium is 300-480 mg, vitamin D should be given 1,000 I.E. at least [50].

References

Select your language of interest to view the total content in your interested language
Post your comment

Share This Article

Recommended Conferences

Article Usage

  • Total views: 8168
  • [From(publication date):
    June-2016 - Dec 17, 2017]
  • Breakdown by view type
  • HTML page views : 8074
  • PDF downloads : 94
 

Post your comment

captcha   Reload  Can't read the image? click here to refresh

Peer Reviewed Journals
 
Make the best use of Scientific Research and information from our 700 + peer reviewed, Open Access Journals
International Conferences 2017-18
 
Meet Inspiring Speakers and Experts at our 3000+ Global Annual Meetings

Contact Us

Agri & Aquaculture Journals

Dr. Krish

[email protected]

1-702-714-7001Extn: 9040

Biochemistry Journals

Datta A

[email protected]

1-702-714-7001Extn: 9037

Business & Management Journals

Ronald

[email protected]

1-702-714-7001Extn: 9042

Chemistry Journals

Gabriel Shaw

[email protected]

1-702-714-7001Extn: 9040

Clinical Journals

Datta A

[email protected]

1-702-714-7001Extn: 9037

Engineering Journals

James Franklin

[email protected]

1-702-714-7001Extn: 9042

Food & Nutrition Journals

Katie Wilson

[email protected]

1-702-714-7001Extn: 9042

General Science

Andrea Jason

[email protected]

1-702-714-7001Extn: 9043

Genetics & Molecular Biology Journals

Anna Melissa

[email protected]

1-702-714-7001Extn: 9006

Immunology & Microbiology Journals

David Gorantl

[email protected]

1-702-714-7001Extn: 9014

Materials Science Journals

Rachle Green

[email protected]

1-702-714-7001Extn: 9039

Nursing & Health Care Journals

Stephanie Skinner

[email protected]

1-702-714-7001Extn: 9039

Medical Journals

Nimmi Anna

[email protected]

1-702-714-7001Extn: 9038

Neuroscience & Psychology Journals

Nathan T

[email protected]

1-702-714-7001Extn: 9041

Pharmaceutical Sciences Journals

Ann Jose

[email protected]

1-702-714-7001Extn: 9007

Social & Political Science Journals

Steve Harry

[email protected]

1-702-714-7001Extn: 9042

 
© 2008- 2017 OMICS International - Open Access Publisher. Best viewed in Mozilla Firefox | Google Chrome | Above IE 7.0 version