scholarly journals Association between Hypomagnesemia, COVID-19, Respiratory Tract and Lung Disease

2021 ◽  
Vol 15 (1) ◽  
pp. 43-45
Author(s):  
Gavino Faa ◽  
Luca Saba ◽  
Daniela Fanni ◽  
Goce Kalcev ◽  
Mauro Carta
Keyword(s):  
Renin Angiotensin System ◽  
Risk Category ◽  
Controlled Trials ◽  
Type I ◽  
Magnesium Supplementation ◽  
Angiotensin System ◽  
Old Adults ◽  
Cd8 T Lymphocytes ◽  
High Risk Category ◽  
Obesity Hypertension

The complexity of COVID-19 is also related to the multiple molecular pathways triggered by SARS-CoV-2, which is able to cause type I pneumocyte death, trigger intravascular coagulation, interfere with the renin-angiotensin system, dysregulate iron metabolism, ending with the insurgence of a cytokine storm which may lead to death. Old adults with obesity, hypertension, and diabetes are among the high-risk category groups more prone to SARS-CoV-2 infection. Magnesium has been reported to play a major role both in physiology and in pathology, particularly in elderly people, regulating cytotoxic functions of natural killer (NK) cells and CD8+ T lymphocytes. In spite of the absence of controlled trials, the possibility of magnesium supplementation for supportive treatment in patients with COVID-19 should be encouraged. This could be useful in all phases of the COVID-19 disease.

scholarly journals The Adipose Renin-Angiotensin System Modulates Systemic Markers of Insulin Sensitivity and Activates the Intrarenal Renin-Angiotensin System

2006 ◽  
Vol 2006 ◽  
pp. 1-6 ◽  
Author(s):  
Suyeon Kim ◽  
Morvarid Soltani-Bejnood ◽  
Annie Quignard-Boulange ◽  
Florence Massiera ◽  
Michele Teboul ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Renin Angiotensin System ◽  
Total Body Weight ◽  
Receptor Protein ◽  
Type I ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Protein Levels ◽  
Total Body ◽  
Plasma Leptin

Background. The adipose tissue renin-angiotensin system (RAS) contributes to regulation of fat mass and may also impact systemic functions such as blood pressure and metabolism.Methods and results. A panel of mouse models including mice lacking angiotensinogen,Agt(Agt-KO), mice expressingAgtsolely in adipose tissue (aP2-Agt/Agt-KO), and mice overexpressingAgtin adipose tissue (aP2-Agt) was studied. Total body weight, epididymal fat pad weight, and circulating levels of leptin, insulin, and resistin were significantly decreased inAgt-KO mice, while plasma adiponectin levels were increased. aP2-Agtmice exhibited increased adiposity and plasma leptin and insulin levels compared to wild type (WT) controls. Angiotensinogen and type I Ang II receptor protein levels were also elevated in kidney of aP2-Agtmice.Conclusion. These findings demonstrate that alterations in adipose RAS activity significantly impact both local and systemic physiology in a way that may contribute to the detrimental health effects of obesity.

Role of the renin-angiotensin system in the pathogenesis of preeclampsia

2005 ◽  
Vol 288 (4) ◽  
pp. F614-F625 ◽  
Author(s):  
Dinesh M. Shah
Keyword(s):  
Angiotensin Ii ◽  
Renin Angiotensin System ◽  
Receptor Activation ◽  
Gravid Uterus ◽  
Type I ◽  
Hypertensive Disorder ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Organ Systems

Preeclampsia is a hypertensive disorder unique to pregnancy with consistent involvement of the kidney. The renin-angiotensin system (RAS) has been implicated in the pathogenesis of preeclampsia. In the gravid state, in addition to the RAS in the kidney, there is a tissue-based RAS in the uteroplacental unit. Increased renin expression observed both in human preeclampsia and in a transgenic mouse model with a human preeclampsia-like syndrome supports the concept that activation of the uteroplacental RAS, with angiotensin II entering the systemic circulation, may mediate the pathogenesis of preeclampsia. A novel disease paradigm of the two-kidney one-clip (2K-1C) Goldblatt model is presented for preeclampsia, wherein the gravid uterus is the clipped “kidney” and the two maternal kidneys represent the unclipped kidney. Validation of the 2K-1C Goldblatt model analogy requires evidence of elevated angiotensin II in the peripheral circulation before vascular maladaptation in preeclampsia. Convincing evidence of the elevation of angiotensin II in preeclampsia does not exist despite the fact that much of vascular pathogenesis appears to be due to angiotensin type I (AT1) receptor activation. Vascular maladaptation with increased vasomotor tone, endothelial dysfunction, and increased sensitivity to angiotensin II and norepinephrine in manifest preeclampsia may be explained on the basis of angiotensin II-mediated mechanisms. Recently, novel angiotensin II-related biomolecular mechanisms have been described in preeclampsia. These include AT1and bradykinin B2receptor heterodimerization and the production of an autoantibody against AT1. Various organ systems with a predilection for involvement in preeclampsia are each a site of a tissue-based RAS. How angiotensin II-mediated mechanisms may explain the primary clinical-pathological features of preeclampsia is described. Future investigations are proposed to more precisely define the role of activation of the uteroplacental RAS in the mechanisms underlying preeclampsia.

scholarly journals GENE polymorphism of the renin angiotensin system in patients with arterial hypertension and coronary heart disease complicated by chronic heart failure

2005 ◽  
Vol 11 (4) ◽  
pp. 235-238
Author(s):  
N. P. Dorofeev ◽  
A. A. Kastanayan ◽  
S. V. Shlyk ◽  
V. V. Dorofeikov ◽  
A. A. Barbina ◽  
...  
Keyword(s):  
Heart Failure ◽  
Coronary Heart Disease ◽  
Heart Disease ◽  
Chronic Heart Failure ◽  
Gene Polymorphism ◽  
Arterial Hypertension ◽  
Renin Angiotensin System ◽  
Type I ◽  
Hypertensive Disease ◽  
Angiotensin System

The purpose of the Study was to search for an association of the gene polymorphism of angiotensin-converting enzyme (ACE), angiotensinogen (ATG) and type I receptors of angiotensin II with the risk for chronic heart failure in patients with coronary heart disease (CHD) and arterial hypertension (AH). A hundred persons, including 80 patients with CHD, 10 patients with hypertensive disease, and 10 healthy Individuals were examined. There was no association of the ID gene polymorphism of ACE, MT gene polymorphism of ATG, and the AC gene polymorphism of ATR1 with the risk for heart failure in patients with CHD and AH.

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