scholarly journals Persistent and selective upregulation of renin–angiotensin system in circulating T lymphocytes in unstable angina

2017 ◽  
Vol 18 (1) ◽  
pp. 147032031769884 ◽  
Author(s):  
Mirella Coppo ◽  
Manuela Bandinelli ◽  
Marco Chiostri ◽  
Loredana Poggesi ◽  
Maria Boddi
Keyword(s):  
T Cells ◽  
T Cell ◽  
Angiotensin Ii ◽  
T Lymphocytes ◽  
Unstable Angina ◽  
Stable Angina ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Ace Activity

Introduction: Unstable angina is associated with an acute systemic inflammatory reaction and circulating T lymphocytes are activated. We investigated whether in unstable angina with marked immune system activation a selective upregulation of the circulating T-cell renin–angiotensin system, modulated by angiotensin II, could occur. Methods: We studied 13 unstable angina patients, 10 patients with stable angina and 10 healthy subjects. After T-lymphocyte isolation, mRNAs for angiotensin-converting enzyme (ACE) and angiotensin type 1 receptor (AT1-R) were quantified at baseline and after angiotensin II stimulation. ACE activity in cell pellet and supernatant and angiotensin II cell content were measured. Results: Plasma renin activity was similar in controls, stable and unstable angina patients. At baseline ACE and AT1-R mRNA levels were higher ( P<0.05) in T cells from unstable angina patients than in T cells from stable angina patients and controls, and further increased after angiotensin II addition to cultured T cells. ACE activity of unstable angina T cells was significantly higher than that of T cells from controls and stable angina patients. Only in T cells from unstable angina patients did angiotensin II stimulation cause the almost complete release of ACE activity in the supernatant. Conclusions: The circulating T-cell-based renin–angiotensin system from unstable angina patients was selectively upregulated. In vivo unstable angina T cells could locally increase angiotensin II concentration in tissues where they migrate independently of the circulating renin–angiotensin system.

Angiotensin II upregulates renin–angiotensin system in human isolated T lymphocytes

2008 ◽  
Vol 151 (1-3) ◽  
pp. 1-6 ◽  
Author(s):  
Mirella Coppo ◽  
Maria Boddi ◽  
Manuela Bandinelli ◽  
Donatella Degl'Innocenti ◽  
Matteo Ramazzotti ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
T Lymphocytes ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin

Vasoactive intestinal peptide down-regulates the intrahepatic renin–angiotensin system in the anaesthetized rat

2000 ◽  
Vol 99 (3) ◽  
pp. 201-206
Author(s):  
V. Z. C. YE ◽  
K. A. DUGGAN
Keyword(s):  
Angiotensin Ii ◽  
Vasoactive Intestinal Peptide ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Sprague Dawley ◽  
Angiotensin I ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Sodium Loading ◽  
Ace Activity

Gastric sodium loading results in an increase in the portal venous concentration of vasoactive intestinal peptide (VIP) and down-regulation of both the intrahepatic and circulating renin–angiotensin systems. In the present study we sought to determine whether an increase in the concentration of VIP in the portal circulation might act to down-regulate the intrahepatic and/or circulating renin–angiotensin systems. Male Sprague–Dawley rats were infused intraportally with haemaccel vehicle or VIP in haemaccel for 60 min. Livers were harvested and blood was sampled. Angiotensin-converting enzyme (ACE) activity and angiotensinogen, angiotensin I, angiotensin II and renin concentrations were measured. VIP infusion decreased hepatic ACE activity (P < 0.05), the hepatic angiotensinogen concentration (P < 0.001) and the hepatic angiotensin I concentration (P < 0.05). The plasma angiotensinogen concentration and serum ACE activity were also decreased by intraportal VIP infusion (P < 0.05 for each). Plasma renin, angiotensin I and angiotensin II concentrations were unchanged by VIP infusion. We conclude that an increase in the portal venous VIP concentration down-regulates the intrahepatic renin–angiotensin system. These changes are similar to those reported after gastric sodium loading, and we suggest, therefore, that the increase in portal venous VIP that occurs after gastric sodium is the means by which the gastric sodium sensor signals the liver to effect these changes in the renin–angiotensin system.

scholarly journals Hypothesis: Free SARS-CoV-2 spike protein S1 particles may act as a factor of COVID-19 pathogenesis.

2020 ◽  
Author(s):  
Andrey Letarov ◽  
Vladislav Babenko
Keyword(s):  
Angiotensin Ii ◽  
Murine Model ◽  
Renin Angiotensin System ◽  
Spike Protein ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Pulmonary Damage ◽  
Infected Cells ◽  
Ace Activity

The disbalance of the renin-angiotensin system was suggested to play an important role in the pathogenesis of the COVID-19 disease. Previously it has been shown that ACE2 expression in downregulated in the murine model in response to SARS-CoV infection and may be also induced by the recombinant spike protein alone. We hypothesize that the soluble SARS-CoV-2 spike protein S1 subunits shed from the infected cells and from the virions in vivo may bind to the ACE2 receptor and trigger ACE2 downregulation. Decreased ACE2 activity on the background of the constant or increased ACE activity in the lungs may lead to the prevalence of angiotensin II effects over angiotensin(1-7) connected to increased thrombosis, inflammation and pulmonary damage.

scholarly journals Pathological Role of Angiotensin II in Severe COVID-19

TH Open ◽  
2020 ◽  
Vol 04 (02) ◽  
pp. e138-e144 ◽  
Author(s):  
Wolfgang Miesbach
Keyword(s):  
Angiotensin Ii ◽  
Angiotensin Converting Enzyme ◽  
Treatment Options ◽  
Renin Angiotensin System ◽  
Target Cells ◽  
Converting Enzyme ◽  
Angiotensin System ◽  
Angiotensin Converting Enzyme 2 ◽  
Renin Angiotensin ◽  
Novel Coronavirus

AbstractThe activated renin–angiotensin system induces a prothrombotic state resulting from the imbalance between coagulation and fibrinolysis. Angiotensin II is the central effector molecule of the activated renin–angiotensin system and is degraded by the angiotensin-converting enzyme 2 to angiotensin (1–7). The novel coronavirus infection (classified as COVID-19) is caused by the new coronavirus SARS-CoV-2 and is characterized by an exaggerated inflammatory response that can lead to severe manifestations such as acute respiratory distress syndrome, sepsis, and death in a proportion of patients, mostly elderly patients with preexisting comorbidities. SARS-CoV-2 uses the angiotensin-converting enzyme 2 receptor to enter the target cells, resulting in activation of the renin–angiotensin system. After downregulating the angiotensin-converting enzyme 2, the vasoconstrictor angiotensin II is increasingly produced and its counterregulating molecules angiotensin (1–7) reduced. Angiotensin II increases thrombin formation and impairs fibrinolysis. Elevated levels were strongly associated with viral load and lung injury in patients with severe COVID-19. Therefore, the complex clinical picture of patients with severe complications of COVID-19 is triggered by the various effects of highly expressed angiotensin II on vasculopathy, coagulopathy, and inflammation. Future treatment options should focus on blocking the thrombogenic and inflammatory properties of angiotensin II in COVID-19 patients.

Renin-angiotensin system and aldosterone secretion during aortic constriction in the rat

1977 ◽  
Vol 232 (5) ◽  
pp. F434-F437 ◽  
Author(s):  
R. H. Freeman ◽  
J. O. Davis ◽  
W. S. Spielman
Keyword(s):  
Angiotensin Ii ◽  
Perfusion Pressure ◽  
Renin Angiotensin System ◽  
Renal Perfusion ◽  
Bilateral Nephrectomy ◽  
Aortic Constriction ◽  
Aldosterone Secretion ◽  
Experimental Conditions ◽  
Angiotensin System ◽  
Renin Angiotensin

Suprarenal aortic constriction sufficient to reduce renal perfusion pressure by approximately 50% increased aldosterone secretion in anesthetized rats pretreated with dexamethasone. Bilateral nephrectomy under the same experimental conditions blocked the aldosterone response. Additionally, [1-sarcosine, 8-alanine]angiotensin II blocked the response in aldosterone secretion to aortic constriction in dexamethasone-treated rats. Finally, in rats hypophysectomized to exclude the influence of ACTH, the aldosterone response to aortic constriction was blocked by [1-sarcosine, 8-alanine]angiotensin II. The results indicate that angiotensin II increased aldosterone secretion during aortic constriction in the rat. These observations, along with those reported previously in sodium-depleted rats, point to an important overall role for the renin-angiotensin system in the control of aldosterone secretion in the rat.

Resveratrol ameliorates the cyclosporine-induced vascular and renal impairments: possible impact of the modulation of renin–angiotensin system

2019 ◽  
Vol 97 (12) ◽  
pp. 1115-1123 ◽  
Author(s):  
Seldag Bekpinar ◽  
Ece Karaca ◽  
Selin Yamakoğlu ◽  
F. İlkay Alp-Yıldırım ◽  
Vakur Olgac ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Angiotensin Converting Enzyme ◽  
Renin Angiotensin System ◽  
Immunosuppressive Drug ◽  
Oxidative Stress Marker ◽  
Converting Enzyme ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
System Components ◽  
Renal Tubular

Cyclosporine, an immunosuppressive drug, exhibits a toxic effect on renal and vascular systems. The present study investigated whether resveratrol treatment alleviates renal and vascular injury induced by cyclosporine. Cyclosporine (25 mg/kg per day, s.c.) was given for 7 days to rats either alone or in combination with resveratrol (10 mg/kg per day, i.p.). Relaxation and contraction responses of aorta were examined. Serum levels of blood urea nitrogen, creatinine, angiotensin II, and angiotensin 1-7 were measured. Histopathological examinations as well as immunostaining for 4-hydroxynonenal and nitrotyrosine were performed in the kidney. RNA expressions of renin–angiotensin system components were also measured in renal and aortic tissues. Cyclosporine decreased the endothelium-dependent relaxation and increased vascular contraction in the aorta. It caused renal tubular degeneration and increased immunostaining for 4-hydroxynonenal, an oxidative stress marker. Cyclosporine also caused upregulations of the vasoconstrictive renin–angiotensin system components in renal (angiotensin-converting enzyme) and aortic (angiotensin II type 1 receptor) tissues. Resveratrol co-treatment prevented the cyclosporine-related deteriorations. Moreover, it induced the expressions of vasodilatory effective angiotensin-converting enzyme 2 and angiotensin II type 2 receptor in aorta and kidney, respectively. We conclude that resveratrol may be effective in preventing cyclosporine-induced renal tubular degeneration and vascular dysfunction at least in part by modulating the renin–angiotensin system.

Sign in / Sign up

Export Citation Format

Share Document