scholarly journals HYPERTENSION IN RELATION TO IMMUNE SYSTEM AND WAY OF LIFE ALONG WITH TREATMENT

2021 ◽  
pp. 1-10
Author(s):  
RAHUL MEHRA ◽  
AANCHAL ◽  
SHAINA KALSI ◽  
SURYA P. GAUTAM
Keyword(s):  
Blood Pressure ◽  
Immune Cell ◽  
Kidney Injury ◽  
Genetically Engineered ◽  
Lifestyle Changes ◽  
Organ Systems ◽  
Genetically Engineered Mice ◽  
The Many ◽  
Hypertension Development ◽  
New Treatments

The objective of the review is to explain the pathophysiology, different causes and various treatments involved in hypertension. This article discusses the disease's pathogenesis, etiology, diagnosis, and immunity. This review looks at the main significant epidemiological and clinical studies on the role of several lifestyle factors in hypertension development. This review examines the numerous mechanisms that cause hypertension in order to discover new treatments. In addition, it covers the many types of hypertension therapy. According to different studies, lifestyle habits may have an impact on blood pressure levels. Moreover, the importance of chronic inflammation in hypertension and its repercussions has been confirmed in genetically engineered mice lacking components of innate and/or adaptive immunity. Immune cell depletion enhances endothelial function, lowers oxidative stress, lowers the vascular tone, and protects against renal interstitial infiltrates, salt retention, and kidney injury. Based on existing literature, there is strong evidence that lifestyle variables can affect blood pressure levels. Then, in hypertensive people, lifestyle changes can help by lowering overall cardiovascular risk and death from any cause. The involvement of immunity as a common thread in the hypertension processes of many organ systems.

scholarly journals miR-146a is a significant brake on autoimmunity, myeloproliferation, and cancer in mice

2011 ◽  
Vol 208 (6) ◽  
pp. 1189-1201 ◽  
Author(s):  
Mark P. Boldin ◽  
Konstantin D. Taganov ◽  
Dinesh S. Rao ◽  
Lili Yang ◽  
Jimmy L. Zhao ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Immune Cell ◽  
Myeloid Cell ◽  
Genetically Engineered ◽  
Biological Processes ◽  
Targeted Deletion ◽  
Genetically Engineered Mice ◽  
Immune Defects ◽  
Molecular Brake

Excessive or inappropriate activation of the immune system can be deleterious to the organism, warranting multiple molecular mechanisms to control and properly terminate immune responses. MicroRNAs (miRNAs), ∼22-nt-long noncoding RNAs, have recently emerged as key posttranscriptional regulators, controlling diverse biological processes, including responses to non-self. In this study, we examine the biological role of miR-146a using genetically engineered mice and show that targeted deletion of this gene, whose expression is strongly up-regulated after immune cell maturation and/or activation, results in several immune defects. Collectively, our findings suggest that miR-146a plays a key role as a molecular brake on inflammation, myeloid cell proliferation, and oncogenic transformation.

The α2-isoform of Na-K-ATPase mediates ouabain-induced hypertension in mice and increased vascular contractility in vitro

2005 ◽  
Vol 288 (2) ◽  
pp. H477-H485 ◽  
Author(s):  
Iva Dostanic ◽  
Richard J. Paul ◽  
John N. Lorenz ◽  
Steven Theriault ◽  
James W. Van Huysse ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Left Ventricular ◽  
Genetically Engineered ◽  
Wild Type ◽  
Vascular Contractility ◽  
Genetically Engineered Mice ◽  
Basal Tone ◽  
Induced Hypertension ◽  
Spontaneous Contractions

Although ouabain is known to induce hypertension, the mechanism of how this cardiac glycoside affects blood pressure is uncertain. The present study demonstrates that the α2-isoform of the Na-K-ATPase mediates the pressor effects of ouabain in mice. To accomplish this, we analyzed the effect of ouabain on blood pressure in wild-type mice, where the α2-isoform is sensitive to ouabain, and genetically engineered mice expressing a ouabain-insensitive α2-isoform of the Na-K-ATPase. Thus differences in the response to ouabain between these two genotypes can only be attributed to the α2-isoform of Na-K-ATPase. As the α1-isoform is naturally resistant to ouabain in rodents, it will not be inhibited by ouabain in either genotype. Whereas prolonged administration of ouabain increased levels of ouabain in serum from both wild-type and targeted animals, hypertension developed only in wild-type mice. In addition, bolus intravenous infusion of ouabain increased the systolic, mean arterial, and left ventricular blood pressure in only wild-type anesthetized mice. In vitro, ouabain increased vascular tone and thereby phenylephrine-induced contraction of the aorta in intact and endothelium-denuded wild-type mice but in α2-resistant mice. Ouabain also increased the magnitude of the spontaneous contractions of portal vein and the basal tone of the intact aorta from only wild-type mice. The increase in aortic basal tone was dependent on the presence of endothelium. Our studies also demonstrate that the α2-isoform of Na-K-ATPase mediates the ouabain-induced increase in vascular contractility. This could play a role in the development and maintenance of ouabain-induced hypertension.

scholarly journals Scnn1Sodium Channel Gene Family in Genetically Engineered Mice

2000 ◽  
Vol 11 (suppl 2) ◽  
pp. S129-S134 ◽  
Author(s):  
EDITH HUMMLER ◽  
FRIEDRICH BEERMANN
Keyword(s):  
Gene Family ◽  
Gene Targeting ◽  
Genetically Engineered ◽  
Channel Gene ◽  
Limiting Step ◽  
Organ Systems ◽  
Genetically Engineered Mice ◽  
Perinatal Lethality ◽  
Targeting Strategy ◽  
A Current

Abstract.The amiloride-sensitive epithelial sodium channel is the limiting step in salt absorption. In mice, this channel is composed of three subunits (α, β, and γ), which are encoded by different genes (Scnn1a, Scnn1b, andScnn1c, respectively). The functions of these genes were recently investigated in transgenic (knockout) experiments, and the absence of any subunit led to perinatal lethality. More defined phenotypes have been obtained by introducing specific mutations or using transgenic rescue experiments. In this report, these approaches are summarized and a current gene-targeting strategy to obtain conditional inactivation of the channel is illustrated. This latter approach will be indispensable for the investigation of channel function in a wide variety of organ systems.

Abstract 175: The Role of Axl in Accumulation of Immune Cells in Kidney and the Onset of Hypertension

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Sri Nagarjun Batchu ◽  
Angie Hughson ◽  
Janice Gerloff ◽  
Deborah J Fowell ◽  
Vyacheslav A Korshunov
Keyword(s):  
Blood Pressure ◽  
Immune Cells ◽  
Immune Cell ◽  
Kidney Injury ◽  
Wild Type ◽  
Protein Levels ◽  
Immune Cell Subsets ◽  
Early Increase ◽  
Salt Hypertension

Introduction: Gas6/Axl pathway contributes to elevation of blood pressure. Immune cells are implicated in initiation and maintenance of hypertension. In this study we aimed to investigate the role of Axl in immune cells on kidney injury and initiation of hypertension. Methods and Results: Deoxycorticosterone-acetate (DOCA; 75mg, 60days release) and salt hypertension was induced for 1wk or 6wks in four groups of Axl chimeras (n=4-5) that were generated by bone marrow (BM) transplant. Multi parameter flow cytometry was used to quantify five major immune cell subsets in digested kidneys from Axl chimeras. Systolic blood pressure (SBP) increased by 30mmHg in Axl+/+ →Axl+/+, Axl-/- →Axl-/- and Axl+/+ →Axl-/- mice after 1wk of DOCA-salt. However, chimeras that lack Axl in the BM cells (Axl-/- →Axl+/+) showed reduction in early increase in SBP (16+2mmHg). We observed a significant decrease in urine protein levels in Axl-/- →Axl+/+ (0.3+0.1μg/μl) compared to other Axl chimeras (∼0.7μg/μl) after 1wk of DOCA-salt. Kidney glomeruli areas were reduced in Axl-/- →Axl+/+ (4,143+229μm 2 ) compared to other Axl chimeras (∼6,000μm 2 ) after 6wks of DOCA-salt. Kidneys from Axl-/- →Axl-/- showed an increase in total leukocytes (8 vs. 4%), B cells (29 vs. 12%) and decrease in monocytes/macrophages (16 vs. 22%) and dendritic cells (5 vs. 10%) compared to Axl+/+ →Axl+/+. Moreover, Axl-/- →Axl+/+ showed further increase in leukocytes (17%), B (39%) and dendritic (13%) cells in kidneys compared to other Axl chimeras. In addition a small percentage of wild type T cells was increased in the kidneys from Axl-/- →Axl+/+ chimeras. Conclusions: These findings suggest that Axl expression in BM-derived cells is critical for kidney injury in DOCA-salt hypertension. Axl-dependent pathways regulate immune cell populations in the kidneys during initiation of hypertension. This study was supported by HL105623 grant (VAK)

scholarly journals The North Karelia Project: Cardiovascular disease prevention in Finland

2018 ◽  
Vol 2018 (2) ◽  
Author(s):  
Erkki Vartiainen
Keyword(s):  
Blood Pressure ◽  
Serum Cholesterol ◽  
Local Population ◽  
Cost Effective ◽  
Population Based ◽  
High Serum ◽  
Lifestyle Changes ◽  
The North ◽  
High Serum Cholesterol ◽  
New Treatments

The extremely high cardiovascular mortality in an eastern province North Karelia in Finland caused great concern among the local population. Action to reduce the problem was demanded in a petition to the Finnish government signed by local representatives of the population. In response, the North Karelia project was launched in 1972 to carry out a comprehensive community based prevention program. After the first five years, prevention activities were also started nationally. The main aim was to reduce the extremely high serum cholesterol, blood pressure and smoking levels with lifestyle changes and improved drug treatment, especially for hypertension. Major declines were seen in serum cholesterol, blood pressure and smoking levels. Coronary mortality reduced in middle age population by 84% from 1972 to 2014. About 2/3 of the mortality decline was explained by risk factor changes and 1/3 by improvement of new treatments developed since 1980s. Population-based prevention through changes in lifestyle and environment is the most cost effective and sustainable way of controlling cardiovascular and other major non-communicable diseases. In the current global situation it is a powerful lesson.

Abstract 065: Induction of Human Endothelin-1 Overexpression for 3 Months Causes Blood Pressure Rise and Renal Injury

Hypertension ◽  
2017 ◽  
Vol 70 (suppl_1) ◽  
Author(s):  
Pierre Paradis ◽  
Suellen C Coelho ◽  
Olga Berillo ◽  
Sofiane Ouerd ◽  
Júlio C Fraulob-Aquino ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Renal Injury ◽  
Immune Cell ◽  
Pressure Rise ◽  
Kidney Injury ◽  
Suppressor Cells ◽  
Dependent Manner ◽  
Artery Flow ◽  
And Control

Introduction: Endothelium-derived endothelin (ET)-1 has been implicated in hypertension and renal disease but the mechanisms are complex and remain unclear. We have shown that tamoxifen-inducible endothelium-restricted human ET-1 overexpressing (ieET-1) mice exhibited BP rise after 3 weeks of induction in an ET type A receptor (ET A R)-dependent manner, in absence of renal injury. It is unknown whether long-term exposure to ET-1 overexpression results in sustained BP elevation and renal injury. Methods: Adult male ieET-1 and control tamoxifen-inducible endothelium-restricted Cre recombinase (ieCre) mice were treated with tamoxifen (1 mg/kg/day, SC) for 5 days and 2.5 months later were treated or not with an ET A R blocker, atrasentan (10 mg/kg/day, PO) for 2 weeks. Blood pressure (BP) by telemetry, renal artery flow (RAF) by ultrasonography, immune cell infiltration by flow cytometry, kidney injury molecule (KIM)-1 expression by immunofluorescence, 24h urinary albumin by ELISA and creatinine by alkaline picrate method were determined at the end of the study. Results: Induction of ET-1 overexpression for 3 months resulted in greater systolic BP (135±4 vs 114±2 mmHg, P <0.001) and reduced RAF (1.7±0.2 vs 3±0.3 mL/min, P <0.05). ieET-1 mice presented increased myeloid (21255±5294 vs 5146±1987 CD11b + cells/kidney, P <0.001) and myeloid-derived suppressor cells (5332±1463 vs 1126±507 CD11b + Gr-1 + cells/kidney, P <0.01) renal infiltration associated with greater frequency of CD11b + (23.2±1.8 vs 7.5±1.6 % of CD45 + cells, P <0.001) and non-immune renal cells (CD45 - , 5.7±0.8 vs 3.2±0.6 % of CD45 - cells, P <0.001) expressing a pro-inflammatory maker, CD36. Early renal injury was demonstrated in ieET-1 by increased KIM-1 expression in proximal tubules (4.0±0.7 vs 1.0±0.2 % of renal cortex, P <0.05) and unchanged albumin/creatinine ratio (327±74 vs 173±36 μg/mg, P=0.215). Atrasentan reversed or reduced all of the above except the decreased RAF ( P <0.05). Conclusions: Long-term exposure to endothelial ET-1 overexpression caused sustained BP elevation and renal injury via ET A R.

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