scholarly journals Immune mechanisms in arterial hypertension. Recent advances

2021 ◽  
Author(s):  
Ulrich O. Wenzel ◽  
Heimo Ehmke ◽  
Marlies Bode
Keyword(s):  
Blood Pressure ◽  
T Cells ◽  
Dendritic Cells ◽  
Immune System ◽  
Organ Damage ◽  
T Cell Subsets ◽  
Blood Pressure Elevation ◽  
End Organ Damage ◽  
Pressure Elevation ◽  
Recent Advances

AbstractIncreasing evidence indicates that hypertension and hypertensive end-organ damage are not only mediated by hemodynamic injury. Inflammation also plays an important role in the pathophysiology and contributes to the deleterious consequences of this disease. Cells of the innate immune system including monocyte/macrophages and dendritic cells can promote blood pressure elevation via effects mostly on kidney and vascular function. Moreover, convincing evidence shows that T and B cells from the adaptive immune system are involved in hypertension and hypertensive end-organ damage. Skin monocyte/macrophages, regulatory T cells, natural killer T cells, and myeloid-derived suppressor cells have been shown to exert blood pressure controlling effects. Sodium intake is undoubtedly indispensable for normal body function but can be detrimental when taken in excess of dietary requirements. Sodium levels also modulate the function of monocyte/macrophages, dendritic cells, and different T cell subsets. Some of these effects are mediated by changes in the microbiome and metabolome that can be found after high salt intake. Modulation of the immune response can reduce severity of blood pressure elevation and hypertensive end-organ damage in several animal models. The purpose of this review is to briefly summarize recent advances in immunity and hypertension as well as hypertensive end-organ damage.

Abstract P3035: Role of T Cells in Sex Differences in Blood Pressure Elevation and Adipose Tissue Expansion Following Chronic High Fat Diet Feeding in Dahl Rats

Hypertension ◽  
2019 ◽  
Vol 74 (Suppl_1) ◽  
Author(s):  
Ahmed A Elmarakby ◽  
Riyaz Mohamed ◽  
Lindsey Ramirez ◽  
Elizabeth Snyder ◽  
Jennifer Sullivan
Keyword(s):  
Blood Pressure ◽  
T Cells ◽  
Sex Differences ◽  
Adipose Tissue ◽  
High Fat Diet ◽  
Tissue Expansion ◽  
High Fat ◽  
Blood Pressure Elevation ◽  
Pressure Elevation

scholarly journals Role of AT1 receptor-mediated salt retention in angiotensin II-dependent hypertension

2011 ◽  
Vol 301 (5) ◽  
pp. F1124-F1130 ◽  
Author(s):  
Steven D. Crowley ◽  
Jiandong Zhang ◽  
Maria Herrera ◽  
Robert Griffiths ◽  
Phillip Ruiz ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Target Organ Damage ◽  
Kidney Injury ◽  
Systemic Blood Pressure ◽  
Organ Damage ◽  
Sodium Reabsorption ◽  
Blood Pressure Elevation ◽  
Pressure Elevation

Activation of type 1 angiotensin II (AT1) receptors in the kidney promotes blood pressure elevation and target organ damage, but whether renal AT1 receptors influence the level of hypertension by stimulating sodium retention or by raising systemic vascular resistance has not been established. In the current studies, we used a kidney cross-transplantation strategy to determine whether increased sodium reabsorption by AT1 receptors in the kidney mediates the chronic hypertensive response to angiotensin II. We found this to be true. In addition, we also identified a second, nontrivial component of blood pressure elevation induced by activation of renal AT1 receptors that is sodium-independent. As the kidney has the capacity to limit the transmission of elevated systemic blood pressure into the renal microcirculation, prior studies struggled to clearly discriminate the relative contributions of blood pressure elevation vs. activation of AT1 receptors to hypertensive kidney injury. In our model, we found that rapid surges in blood pressure, which may overcome the kidney's capacity to prevent perturbations in renal hemodynamics, correlate closely with kidney damage in hypertension. Moreover, maximal kidney injury in hypertension may require activation of a pool of nonrenal, systemic AT1 receptors. These studies provide insight into precise mechanisms through which AT1 receptor blockade influences the progression of hypertensive kidney disease.

scholarly journals Memories that last in hypertension

2015 ◽  
Vol 308 (11) ◽  
pp. F1197-F1199 ◽  
Author(s):  
Hana A. Itani ◽  
David G. Harrison
Keyword(s):  
T Cells ◽  
Memory T Cells ◽  
Vascular Dysfunction ◽  
Organ Damage ◽  
Interferon Γ ◽  
T Cell Subsets ◽  
Distal Nephron ◽  
Blood Pressure Elevation ◽  
Memory T Cell ◽  
Specific Memory

In recent years, it has become clear that the immune system contributes to the genesis of hypertension. Hypertensive stimuli, such as angiotensin II, DOCA-salt, and norepinephrine, cause T cells and monocytes/macrophages to accumulate in the kidney and vasculature. These cells release inflammatory cytokines, such as IL-6, interferon-γ, and IL-17, that promote renal and vascular dysfunction. These cytokines also promote angiotensinogen production in the proximal tubule and Na+ retention in the distal nephron and contribute to renal fibrosis and glomerular damage. For several years, we have observed accumulation of memory T cells in the kidney and vasculature. Given the propensity for memory cells to produce cytokines such as interferon-γ and IL-17, interventions to prevent the formation or renal accumulation of specific memory T cell subsets could prevent end-organ damage and blood pressure elevation in response to hypertensive stimuli.

Immune mechanisms in hypertension and vascular injury

2013 ◽  
Vol 126 (4) ◽  
pp. 267-274 ◽  
Author(s):  
Ernesto L. Schiffrin
Keyword(s):  
Blood Pressure ◽  
Cardiovascular Disease ◽  
T Cells ◽  
Treg Cells ◽  
Interleukin 17 ◽  
Low Grade ◽  
Vascular Remodelling ◽  
Blood Pressure Elevation ◽  
Immune Mechanisms ◽  
Pressure Elevation

Over the last 20 years it has become recognized that low-grade inflammation plays a role in cardiovascular disease. More recently, participation of the innate and the adaptive immune response in mechanisms that contribute to inflammation in cardiovascular disease has been reported in atherosclerosis and hypertension. Different subsets of lymphocytes and their cytokines are involved in vascular remodelling in hypertension, chronic kidney disease and heart disease. Effector T-cells include Th1 (interferon-γ-producing) and Th2 (interleukin-4 producing) lymphocytes, as well as Th17 (which produce interleukin-17) and T-suppressor lymphocytes such as Treg-cells (regulatory T-cells), which express the transcription factor Foxp3 (forkhead box P3) and participate respectively as pro- and anti-inflammatory cells. Pro-inflammatory T-lymphocytes participate in mechanisms of cardiovascular disease in part by mediating the effects of angiotensin II and mineralocorticoids. Involvement of immune mechanisms in cardiac, vascular and renal changes in hypertension has been demonstrated in many experimental models, an example being the Dahl-salt sensitive rat and the spontaneously hypertensive rat. How activation of immunity is triggered remains unknown, but neo-antigens could be generated by elevated blood pressure through damage-associated molecular pattern receptors or other mechanisms. Once activated, Th1 cells may contribute to blood pressure elevation by affecting the kidney, vascular remodelling of blood vessels directly via the effects of the cytokines produced or through their effects on perivascular fat. Treg-cells protect from blood pressure elevation by acting upon similar targets. Recent data suggests that participation of these mechanisms that have been demonstrated already in murine models also occurs in humans. These novel findings may open the way for new therapeutic approaches to improve outcomes in hypertension and cardiovascular disease in humans.

scholarly journals Új szempontok a sószenzitív hypertoniák patomechanizmusában

2019 ◽  
Vol 160 (2) ◽  
pp. 43-49
Author(s):  
Endre Sulyok
Keyword(s):  
Blood Pressure ◽  
Extracellular Space ◽  
Salt Intake ◽  
Sodium Intake ◽  
Organ Damage ◽  
Blood Pressure Elevation ◽  
High Sodium ◽  
End Organ Damage ◽  
Inactive Form ◽  
Factor C

Abstract: This article shortly outlines the evolution of hypertonia from risk factors to end-organ damage. The pathogenetic role of salt intake is underlined and in the light of recent clinical and experimental observations, the importance of renal and extrarenal mechanism in the development of salt-sensitive hypertension is analysed. The generally accepted concept that the inefficient renal sodium excretion and the subsequent expansion of the extracellular space is the major factor in blood pressure elevation is challenged. Evidences have been provided that the retained sodium dissociates from the volume of extracellular space and, also from the blood pressure. It has been shown that the negatively charged macromolecules in the subcutaneous interstitium bind sodium ions in osmotically inactive form and store sodium reversibly. The local tissue hypertonicity induces monocytes/macrophages invasion and activation that causes increased expression of tonicity-responsive enhancer binding protein (TonEBP) and the secretion of vascular endothelial growth factor C that result in enhanced lymphangiogenesis. The expanded lymphatic system drains the excess sodium and volume back to the circulation. The reduction of buffer function of this system may contribute to the development or to worsening of hypertension. Similar buffer and barrier functions are attributed to the glycocalyx that covers the luminal surface of vascular endothelium. It is also recognised that the high sodium intake alone is an important pathogenetic factor in end-organ damage independent of hypertension. This may be accounted for by the induction and activation of Th17 cells as well as by the increased production of several pro-inflammatory and pro-fibrotic cytokines. Orv Hetil. 2019; 160(2): 43–49.

Abstract 043: Dendritic Cells Mediate Renal T Cell Activation in Hypertension

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Nathan P Rudemiller ◽  
Jiandong Zhang ◽  
Gianna E Hammer ◽  
Yen-Rei A Yu ◽  
Robert Griffiths ◽  
...  
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
T Cell ◽  
T Cell Activation ◽  
Cell Activation ◽  
Immune Cell ◽  
Effector T Cells ◽  
T Cell Subsets ◽  
Ang Ii ◽  
Blood Pressure Elevation

Activated T lymphocytes exacerbate hypertension in part by infiltrating the kidney to promote sodium retention. Dendritic cells (DCs) are the most potent antigen presenting cells that activate T cells and have been shown to contribute to hypertension. The current studies therefore explored whether DC-mediated activation of renal T cells can exaggerate the chronic hypertensive response to angiotensin (Ang) II. First, we confirmed that renal T cells undergo DC-mediated activation during the initiation of hypertension by analyzing immune cell populations in renal tissue via flow cytometry. In Fms-like tyrosine kinase 3 ligand-deficient (FLT3L KO) mice that lack DCs, the proportions of effector (CD44 hi CD62 lo ) T cells in the kidney were similar to wild-type (WT) controls at baseline (50±3 vs. 52±7% of CD3 + cells). However, after 5 days of Ang II-induced hypertension, the proportions of effector T cells were dramatically higher in the WT kidney versus the FLT3L KOs (69±3 vs. 52±3% of CD3 + cells; p<0.01), indicating that DCs activate T cells in hypertension. As DCs activate T cells in local lymph nodes, we phenotyped T cell subsets in the kidney lymph node (KLN) following 4 weeks of hypertension and detected elevated proportions of effector CD4 + T cells compared to baseline (10.7±2.0 vs. 6.9±0.8% of CD4 + T cells). The ubiquitin-editing protein A20 in DCs suppresses their capacity to stimulate T cells. Thus, mice with heterozygous deletion of A20 in DCs (CD11c-cre A20 flox/wt = DC ACT) harbor spontaneously active DCs that enhance T cell activation. To test the contribution of DC-mediated T cell activation to hypertension, we measured blood pressures in WT and DC ACT mice during 4 weeks of chronic Ang II infusion (300ng/kg/min). While MAPs were similar in the 2 groups at baseline, the DC ACT mice had an exaggerated chronic hypertensive response (143±2 vs. 131±4 mmHg; p=0.04) with more severe cardiac hypertrophy (7.3±0.3 vs. 6.4±0.4 mg/gm body wt; p<0.04). The KLNs from the DC ACT animals also contained higher proportions of effector T cells than controls (12.1±0.2 vs. 8.2±0.5% of CD3 + cells; p<0.01). In conclusion, DC-mediated activation of T cells promotes blood pressure elevation by facilitating the accumulation of effector T cells in the kidney during hypertension.

Role of the Autonomic Nervous System in the Acute Blood Pressure Elevation during Repetitive Hypoxic and Hypercapnic Breathing in Rats

1996 ◽  
Vol 5 (6) ◽  
pp. 371-375 ◽  
Author(s):  
M. Bakehe ◽  
J. Hedner ◽  
T. Dang ◽  
B. Chambille ◽  
C. L. Gaultier ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Autonomic Nervous System ◽  
Blood Pressure Elevation ◽  
Autonomic Nervous ◽  
Pressure Elevation
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