Abstract P265: Hypertension, Vascular Dysfunction And Downregulation Of The Renin Angiotensin System Sequelae Of COVID-19

Hypertension ◽  
2021 ◽  
Vol 78 (Suppl_1) ◽  
Author(s):  
Linsay McCallum ◽  
Stefanie Lip ◽  
Francisco J Rios ◽  
Karla B Neves ◽  
Jason Kilmartin ◽  
...  
Keyword(s):  
Vascular Dysfunction ◽  
Vascular Inflammation ◽  
Renin Angiotensin System ◽  
Tnf Alpha ◽  
Post Discharge ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Multivariable Regression ◽  
Cv Disease ◽  
Multivariable Regression Models

Hypertension, vascular dysfunction and downregulation of the renin angiotensin system as sequelae of COVID-19 The long-term CV consequences of COVID are unknown however the potential for ongoing cardiac and vascular inflammation with RAAS alteration may increase the risk of developing hypertension and CV disease. Non-hypertensive patients hospitalised in April-May 2020 with either confirmed COVID19 (cases) or non-COVID (controls) diagnosis were recruited ≥12 weeks post-discharge. All underwent detailed BP and vascular/immune and RAAS phenotyping. The primary outcome was ABPM 24-hr SBP. Paired t-tests and multivariable regression models used to assess differences. Thirty cases and eighteen controls completed the study. Cases were older (51±7 vs 45±9 years) with lower discharge SBP (121±10 vs 128±15 mmHg; p0.01). ABPM at study visit was higher in the cases compared to controls (24-hour SBP (OR[95%CI]: 8.6[0.9-16.3]; p0.03), day-time SBP (8.6[1.5-17.3]; p0.02), day-time DBP (4.6[0.1-9.1]; p<0.05). Paired analysis of office BP showed a 11 mmHg difference between cases and controls (11.5[3.12];19.8; p=0.008; figure) Cases had lowerRenin and Ang-1-10 levels (-0.4[-0.9-0.1]; p0.08; -0.7[-1.2- -0.1]; p0.02 respectively) and higher TNF-alpha (0.5[0.1-0.9]; p0.01). Confirmed COVID requiring hospitalisation is associated with elevated SBP, reduced renin and Ang-1-10 and elevated TNF-alpha at ≥12 weeks post-discharge.

scholarly journals Role of Renin-Angiotensin System and Oxidative Stress on Vascular Inflammation in Insulin Resistence Model

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
N. F. Renna ◽  
C. Lembo ◽  
E. Diez ◽  
R. M. Miatello
Keyword(s):  
Oxidative Stress ◽  
Experimental Model ◽  
Chronic Treatment ◽  
Vascular Tissue ◽  
Vascular Inflammation ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
The Creation ◽  
And Oxidative Stress

(1) This study aims to demonstrate the causal involvement of renin angiotensin system (RAS) and oxidative stress (OS) on vascular inflammation in an experimental model of metabolic syndrome (MS) achieved by fructose administration to spontaneously hypertensive rats (FFHR) during 12 weeks. (2) Chronic treatment with candesartan (C) (10 mg/kg per day for the last 6 weeks) or 4OH-Tempol (T) (10−3 mmol/L in drinking water for the last 6 weeks) reversed the increment in metabolic variables and systolic blood pressure. In addition, chronic C treatment reverted cardiovascular remodeling but not T. (3) Furthermore, chronic treatment with C was able to completely reverse the expression of NF-κB and VCAM-1, but T only reduced the expression. C reduced the expression of proatherogenic cytokines as CINC2, CINC3, VEGF, Leptin, TNF-alpha, and MCP-1 and also significantly reduced MIP-3, beta-NGF, and INF-gamma in vascular tissue in this experimental model. T was not able to substantially modify the expression of these cytokines. (4) The data suggest the involvement of RAS in the expression of inflammatory proteins at different vascular levels, allowing the creation of a microenvironment suitable for the creation, perpetuation, growth, and destabilization of vascular injury.

scholarly journals The world pandemic of vitamin D deficiency could possibly be explained by cellular inflammatory response activity induced by the renin-angiotensin system

2013 ◽  
Vol 304 (11) ◽  
pp. C1027-C1039 ◽  
Author(s):  
Marcelo Ferder ◽  
Felipe Inserra ◽  
Walter Manucha ◽  
León Ferder
Keyword(s):  
Vitamin D ◽  
Vascular Inflammation ◽  
Renin Angiotensin System ◽  
Left Ventricular ◽  
Point Of View ◽  
The Other ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Immunological Mechanisms ◽  
Cellular Inflammatory Response

This review attempts to show that there may be a relationship between inflammatory processes induced by chronic overstimulation of the renin-angiotensin system (RAS) and the worldwide deficiency of vitamin D (VitD) and that both disorders are probably associated with environmental factors. Low VitD levels represent a risk factor for several apparently different diseases, such as infectious, autoimmune, neurodegenerative, and cardiovascular diseases, as well as diabetes, osteoporosis, and cancer. Moreover, VitD insufficiency seems to predispose to hypertension, metabolic syndrome, left ventricular hypertrophy, heart failure, and chronic vascular inflammation. On the other hand, inappropriate stimulation of the RAS has also been associated with the pathogenesis of hypertension, heart attack, stroke, and hypertrophy of the left ventricle and vascular smooth muscle cells. Because VitD receptors (VDRs) and RAS receptors are almost distributed in the same tissues, a possible link between VitD and the RAS is even more plausible. Furthermore, from an evolutionary point of view, both systems were developed simultaneously, actively participating in the regulation of inflammatory and immunological mechanisms. Changes in RAS activity and activation of the VDR seem to be inversely related; thus any changes in one of these systems would have a completely opposite effect on the other, making it possible to speculate that the two systems could have a feedback relationship. In fact, the pandemic of VitD deficiency could be the other face of increased RAS activity, which probably causes lower activity or lower levels of VitD. Finally, from a therapeutic point of view, the combination of RAS blockade and VDR stimulation appears to be more effective than either RAS blockade or VDR stimulation individually.

Role of the renin–angiotensin system in vascular inflammation

2008 ◽  
Vol 29 (7) ◽  
pp. 367-374 ◽  
Author(s):  
Chiara Marchesi ◽  
Pierre Paradis ◽  
Ernesto L. Schiffrin
Keyword(s):  
Vascular Inflammation ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin

Abstract P205: Endothelium-specific Interference with PPARG Causes Cerebral Vascular Dysfunction in Response to Endogenous Renin-angiotensin System Activation

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Anand R Nair ◽  
Masashi Mukohda ◽  
Larry N Agbor ◽  
Chunyan Hu ◽  
Jing Wu ◽  
...  
Keyword(s):  
Carotid Artery ◽  
Basilar Artery ◽  
Vascular Dysfunction ◽  
Renin Angiotensin System ◽  
Dominant Negative ◽  
Angiotensin System ◽  
Salt Diet ◽  
Renin Angiotensin ◽  
Ras Activation ◽  
Low Salt

Abnormal activation of the endogenous renin-angiotensin system (RAS) has been implicated in various cardiovascular (CV) disorders including hypertension, atherosclerosis and stroke. Whereas a low salt diet may be beneficial in salt-sensitive hypertension, it has been proposed to also cause CV risk due to activation of the RAS. The molecular mechanism by which RAS activation mediates vascular dysfunction remains undefined. Peroxisome proliferator-activated receptor gamma (PPARγ) is a ligand-activated transcription factor which activates anti-oxidant and anti-inflammatory processes and can regulate the actions of angiotensin II (AngII) in the vasculature. We examined endothelial function in transgenic mice specifically expressing dominant-negative (DN) mutations in PPARγ in the endothelium (E-V290M) fed a low salt diet to test the hypothesis that endothelial PPARγ plays a protective role in the vasculature in response to endogenous RAS activation. Circulating levels of renin were significantly increased in both non-transgenic (NT) and E-V290M mice fed a low-salt diet for 6 weeks compared to standard chow (NT: 39.3±7.4 vs 19.8±1.3 ng/ml; E-V290M: 34.3±0.8 vs 16.0±3.8 ng/ml, p<0.05, n=5). Under baseline conditions, responses to endothelium-dependent agonist acetylcholine were not affected in E-V290M mice compared to NT (basilar artery: 66.1±11.8 vs 63.5±3.7%; carotid artery: 93.3±3.6 vs 91.1±4.2%, n=5). Six weeks of low-salt diet significantly impaired acetylcholine-mediated dilation in the basilar artery of E-V290M mice but not in NT (41.7±7.7 vs 74.2±5.0%, p<0.05, n=5). Unlike basilar artery, 6 weeks of low salt diet was not sufficient to induce vascular dysfunction in carotid artery or aorta of E-V290M mice (carotid artery: 85.6±4.4 vs 91.9±2.5%, n=5; aorta: 80.8±5.4 vs 87.0±5.6%, n=3). The responses to endothelium-independent vasodilator sodium nitroprusside (SNP) were not different in E-V290M mice compared to NT controls. We conclude that endothelial-specific interference with PPARγ causes endothelial dysfunction in response to endogenous RAS activation induced by a low-salt diet. Moreover, the cerebral circulation is particularly susceptible to low salt diet-induced dysfunction in conjunction with PPARγ impairment.

TNF Alpha-308 Genotype and Renin-Angiotensin System in Hemodialysis Patients: An Effect on Inflammatory Cytokine Levels?

2005 ◽  
Vol 29 (2) ◽  
pp. 174-178 ◽  
Author(s):  
Gultekin Genctoy ◽  
Bulent Altun ◽  
Ahmet Alper Kiykim ◽  
Mustafa Arici ◽  
Yunus Erdem ◽  
...  
Keyword(s):  
Inflammatory Cytokine ◽  
Renin Angiotensin System ◽  
Hemodialysis Patients ◽  
Tnf Alpha ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Cytokine Levels

scholarly journals Renin–angiotensin system overactivation in perivascular adipose tissue contributes to vascular dysfunction in heart failure

2020 ◽  
Vol 134 (23) ◽  
pp. 3195-3211
Author(s):  
Milene Tavares Fontes ◽  
Suliana Mesquita Paula ◽  
Caroline Antunes Lino ◽  
Nathalia Senger ◽  
Gisele Kruger Couto ◽  
...  
Keyword(s):  
Heart Failure ◽  
Adipose Tissue ◽  
Angiotensin Ii ◽  
Thoracic Aorta ◽  
Vascular Dysfunction ◽  
Renin Angiotensin System ◽  
Angiotensin Ii Receptor ◽  
Perivascular Adipose Tissue ◽  
Angiotensin System ◽  
Renin Angiotensin

Abstract Perivascular adipose tissue (PVAT) dysfunction is associated with vascular damage in cardiometabolic diseases. Although heart failure (HF)-induced endothelial dysfunction is associated with renin–angiotensin system (RAS) activation, no data have correlated this syndrome with PVAT dysfunction. Thus, the aim of the present study was to investigate whether the hyperactivation of the RAS in PVAT participates in the vascular dysfunction observed in rats with HF after myocardial infarction surgery. Wire myograph studies were carried out in thoracic aorta rings in the presence and absence of PVAT. An anticontractile effect of PVAT was observed in the rings of the control rats in the presence (33%) or absence (11%) of endothelium. Moreover, this response was substantially reduced in animals with HF (5%), and acute type 1 angiotensin II receptor (AT1R) and type 2 angiotensin II receptor (AT2R) blockade restored the anticontractile effect of PVAT. In addition, the angiotensin-converting enzyme 1 (ACE1) activity (26%) and angiotensin II levels (51%), as well as the AT1R and AT2R gene expression, were enhanced in the PVAT of rats with HF. Associated with these alterations, HF-induced lower nitric oxide bioavailability, oxidative stress and whitening of the PVAT, which suggests changes in the secretory function of this tissue. The ACE1/angiotensin II/AT1R and AT2R axes are involved in thoracic aorta PVAT dysfunction in rats with HF. These results suggest PVAT as a target in the pathophysiology of vascular dysfunction in HF and provide new perspectives for the treatment of this syndrome.

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