scholarly journals The Role of Angiotensin Antagonism in Coronary Plaque Regression: Insights from the Glagovian Model

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Abdul H. Alkatiri ◽  
Dony Firman ◽  
Amir A. Alkatiri ◽  
Paskalis I. Suryajaya ◽  
Albert Sudharsono
Keyword(s):  
Angiotensin Ii ◽  
Enzyme Inhibitor ◽  
Basic Mechanism ◽  
Coronary Plaque ◽  
Vital Role ◽  
Atheromatous Plaque ◽  
Arterial Remodeling ◽  
Plaque Regression ◽  
Artery Disease

The benefit of antagonizing the effect of the renin angiotensin aldosterone system (RAAS), notably by the use of angiotensin-converting enzyme inhibitor (ACEi) and angiotensin II type 1 receptor blocker (ARB) for coronary artery disease (CAD), has been demonstrated in multiple studies, which may be attributed to their ability to inhibit the deleterious effect of RAAS to the cardiovascular system. It is well known that angiotensin II (Ang II) plays a vital role in atheromatous plaque formation and progression through multiple pathways, including inflammatory and arterial remodeling aspects. Significant coronary atheromatous plaque regression has been previously demonstrated in various studies using statin agents. Similar results have been reported in different studies using angiotensin inhibitor agents, notably ARB agents. Analysis from various trials utilizing ARB showed a significant plaque regression using olmesartan and telmisartan as evaluated by IVUS studies. In contrary, the use of ACEi did not demonstrated significant plaque regression, which may be attributed to the heavy plaque calcification in respective studies. On this review, we aim to present the basic mechanism on the role of RAAS in plaque modulation and its arterial remodeling aspect, which is then integrated with the clinical evidence based on the available intravascular ultrasonography (IVUS) studies on coronary arteries.

Understanding the role of Inflammasome in Angina Pectoris

2020 ◽  
Vol 21 ◽  
Author(s):  
Ishita Sharma ◽  
Tapan Behl ◽  
Simona Bungau ◽  
Monika Sachdeva ◽  
Arun Kumar ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Angina Pectoris ◽  
Nlrp3 Inflammasome ◽  
Vital Role ◽  
Death Process ◽  
Cell Death Process ◽  
Artery Disease ◽  
Species Production ◽  
Pro Inflammatory Cytokines

Abstract:: Angina pectoris, associated with coronary artery disease, a cardiovascular disease where, pain is caused by adverse oxygen supply in myocardium, resulting in contractility and discomfort in chest. Inflammasomes, triggered by stimuli due to infection and cellular stress have identified to play a vital role in the progression of cardiovascular disorders and thus, causing various symptoms like angina pectoris. Nlrp3 inflammasome, a key contributor in the pathogenesis of angina pectoris, requires activation and primary signaling for the commencement of inflammation. Nlrp3 inflammasome elicit out an inflammatory response by emission of pro inflammatory cytokines by ROS (reactive oxygen species) production, mobilization of K+ efflux and Ca2+ and by activation of lysosome destabilization that eventually causes pyroptosis, a programmed cell death process. Thus, inflammasome are considered to be one of the factors involved in the progression of coronary artery diseases and have an intricate role in development of angina pectoris.

Renal hemodynamic responses to increased renal venous pressure: role of angiotensin II

1982 ◽  
Vol 243 (3) ◽  
pp. F260-F264 ◽  
Author(s):  
P. R. Kastner ◽  
J. E. Hall ◽  
A. C. Guyton
Keyword(s):  
Angiotensin Ii ◽  
Filtration Rate ◽  
Enzyme Inhibitor ◽  
Venous Pressure ◽  
Renin Secretion ◽  
Ang Ii ◽  
Converting Enzyme ◽  
Filtration Fraction ◽  
A Value

Studies were performed to quantitate the effects of progressive increases in renal venous pressure (RVP) on renin secretion (RS) and renal hemodynamics. RVP was raised in 10 mmHg increments to 50 mmHg. Renin secretion rate increased modestly as RVP was increased to 30 mmHg and then increased sharply after RVP exceeded 30 mmHg. Glomerular filtration rate (GFR), renal blood flow (RBF), and filtration fraction (FF) did not change significantly when RVP was elevated to 50 mmHg. GFR and RBF were also measured after the renin-angiotension system (RAS) was blocked with the angiotensin converting enzyme inhibitor (CEI) SQ 14225. After a 60-min CEI infusion, RBF was elevated (32%), GFR was unchanged, FF was decreased, and total renal resistance (TRR) was decreased. As RVP was increased to 50 mmHg, GFR and FF decreased to 36.3 and 40.0% of control, respectively, RBF returned to a value not significantly different from control, and TRR decreased to 44.8% of control. The data indicate that the RAS plays an important role in preventing reductions in GFR during increased RVP because blockade of angiotensin II (ANG II) formation by the CEI results in marked decreases in GFR at high RVPs. The decreases in GFR after ANG II blockade and RVP elevation were not due to lack of renal vasodilation, since TRR was maintained below while RBF was maintained either above or at the pre-CEI levels.

Thermal responses to central angiotensin II, SQ 20881, and dopamine infusions in sheep

1985 ◽  
Vol 248 (3) ◽  
pp. R371-R377 ◽  
Author(s):  
B. S. Huang ◽  
M. J. Kluger ◽  
R. L. Malvin
Keyword(s):  
Angiotensin Ii ◽  
Body Temperature ◽  
Enzyme Inhibitor ◽  
Renin Angiotensin System ◽  
Significant Rise ◽  
Ang Ii ◽  
Deep Body Temperature ◽  
Angiotensin System ◽  
Conscious Sheep

The thermoregulatory role of brain angiotensin II (ANG II) was tested by intracerebroventricular (IVT) infusion of ANG II or the converting enzyme inhibitor SQ 20881 (SQ) in 15 conscious sheep. Deep body temperature decreased 0.30 +/- 0.07 degree C (SE) during the 3-h period of IVT ANG II (25 ng/min) infusion (P less than 0.05) and increased 0.50 +/- 0.13 degree C during IVT SQ (1 microgram/min) infusion (P less than 0.01). To determine whether the rise in body temperature after IVT SQ infusion might be the result of a central renin-angiotensin system (RAS), SQ was infused IVT in five conscious sheep 20 h after bilateral nephrectomy. This resulted in a significant rise in body temperature of 0.28 +/- 0.05 degree C (P less than 0.05). When vasopressin antidiuretic hormone (ADH) was infused intravenously at the same time of IVT SQ infusion, the rise in temperature was depressed, but ADH did not lower the temperature below basal. IVT dopamine (20 micrograms/min) increased body temperature by 0.40 +/- 0.04 degree C (P less than 0.01), which was qualitatively similar to the result with IVT SQ. These data support the hypothesis that endogenous brain ANG II may play a role in thermoregulation. Furthermore, plasma ADH level, regulated in part by brain ANG II, is probably not the mediator of that thermoregulation. The similar effects of IVT dopamine and SQ on body temperature strengthen the hypothesis that dopamine may be involved in the central action of brain ANG II.

Role of arteria baroreceptor input on thirst and urinary responses to intracerebroventricular angiotensin II

1993 ◽  
Vol 265 (3) ◽  
pp. R591-R595 ◽  
Author(s):  
R. L. Thunhorst ◽  
S. J. Lewis ◽  
A. K. Johnson
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Arterial Blood Pressure ◽  
Water Intake ◽  
Enzyme Inhibitor ◽  
Ang Ii ◽  
Converting Enzyme ◽  
Arterial Blood ◽  
Endogenous Formation

Intracerebroventricular (icv) infusion of angiotensin II (ANG II) in rats elicits greater water intake under hypotensive, compared with normotensive, conditions. The present experiments used sinoaortic baroreceptor-denervated (SAD) rats and sham-operated rats to examine if the modulatory effects of arterial blood pressure on water intake in response to icv ANG II are mediated by arterial baroreceptors. Mean arterial blood pressure (MAP) was raised or lowered by intravenous (i.v.) infusions of phenylephrine (1 or 10 micrograms.kg-1 x min-1) or minoxidil (25 micrograms.kg-1 x min-1), respectively. The angiotensin-converting enzyme inhibitor captopril (0.33 mg/min) was infused i.v. to prevent the endogenous formation of ANG II during testing. Urinary excretion of water and solutes was measured throughout. Water intake elicited by icv ANG II was inversely related to changes in MAP. Specifically, rats drank more water in response to icv ANG II when MAP was reduced by minoxidil but drank less water when MAP was elevated by phenylephrine. The influence of changing MAP on the icv ANG II-induced drinking responses was not affected by SAD. These results suggest that the modulatory effects of arterial blood pressure on icv ANG II-induced drinking can occur in the absence of sinoaortic baroreceptor input.

Stimulation of aldosterone biosynthesis by sodium sequestration: role of angiotensin II

1982 ◽  
Vol 243 (6) ◽  
pp. E450-E457
Author(s):  
J. Muller ◽  
E. G. Lund ◽  
L. Hofstetter ◽  
D. B. Brunner ◽  
P. Haldy
Keyword(s):  
Angiotensin Ii ◽  
Enzyme Inhibitor ◽  
Zona Glomerulosa ◽  
High Dose ◽  
Converting Enzyme ◽  
Bilateral Nephrectomy ◽  
Stimulatory Action ◽  
Sodium Sequestration ◽  
Stimulation Of

The role of angiotensin II in the stimulation of aldosterone biosynthesis by sodium sequestration in potassium-deficient rats was assessed by experiments involving 1-day angiotensin II infusion, converting enzyme inhibition, and bilateral nephrectomy. In intact rats, only an extremely high dose of exogenous angiotensin II imitated the stimulatory effects of polyethylene glycol-induced edema on the conversions of deoxycorticosterone and corticosterone to 18-hydroxycorticosterone and aldosterone. Treatment with the converting enzyme inhibitor captopril as well as bilateral nephrectomy blocked the aldosterone-stimulating action of edema. This inhibition was prevented by the simultaneous infusion of angiotensin II in captopril-treated rats but not in nephrectomized animals. According to these results, angiotensin II is an essential mediator in the stimulation of aldosterone biosynthesis by sodium sequestration. However, the role of the kidneys appears to be twofold. First, they act through the secretion of renin. In addition, a second yet unknown kidney factor is necessary for a full response of the zona glomerulosa to the stimulatory action of angiotensin II.

scholarly journals Role of the Angiotensin II Type 2 Receptor in Arterial Remodeling after Wire Injury in Mice

2008 ◽  
Vol 31 (6) ◽  
pp. 1241-1249 ◽  
Author(s):  
Yoshiyuki YAMAMOTO ◽  
Yuichiro WATARI ◽  
Andrei BRYDUN ◽  
Masao YOSHIZUMI ◽  
Masahiro AKISHITA ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Arterial Remodeling

Serum chromium and angiographically determined coronary artery disease.

1978 ◽  
Vol 24 (4) ◽  
pp. 541-544 ◽  
Author(s):  
H A Newman ◽  
R F Leighton ◽  
R R Lanese ◽  
N A Freedland
Keyword(s):  
Risk Factors ◽  
Blood Pressure ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Plaque Formation ◽  
Atheromatous Plaque ◽  
Lower Serum ◽  
Serum Chromium ◽  
Artery Disease

Abstract Human aortas sampled from populations where there is little advanced atheromatous plaque formation contain higher concentrations of chromium than do aortas from populations in which atheromatosis is prevalent. In the present study serum cholesterol, triacylglycerols, and chromium (Cr3+) concentrations were measured in 32 subjects in whom coronary artery disease was assessed by cineangiography. The distribution of subjects with diseased and normal arteries overlapped below 5.50 microgram of chromium per liter. Only subjects free of coronary artery disease had chromium concentrations greater than or equal to 5.50 microgram/liter. The role of chromium was assessed in the context of the selected risk factors: cholesterol, triacylglycerols, and systolic and diastolic blood pressure. The group with coronary artery disease had significantly lower serum chromium concentrations than did the group with normally patent arteries.

Abstract 301: Angiotensin II-induced Aortic Stiffening is Associated With Upregulation of Mir-21 And Downregulation of Mir-29b

2013 ◽  
Vol 33 (suppl_1) ◽  
Author(s):  
Uwe Raaz ◽  
Ryuji Toh ◽  
Matti Adam ◽  
Futoshi Nakagami ◽  
Lars Maegdefessel ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Angiotensin Ii ◽  
Infrarenal Aorta ◽  
Arterial Remodeling ◽  
Fibrotic Response ◽  
Arterial Stiffening ◽  
Small Noncoding Rnas ◽  
Aortic Stiffening

Background Arterial stiffening is associated with aging, as well as numerous diseases such as hypertension, congestive heart failure, diabetes mellitus and renal failure, and has been identified as an independent risk factor for cardiovascular disease. Consequently there is a growing interest in the mechanisms that govern the process of arterial remodeling. Recently, small noncoding RNAs, termed microRNAs (miRs), have emerged as powerful cellular regulators involved in disease and tissue remodeling. More specifically, miR-29b downregulation as well as miR-21 upregulation have been identified as pro-fibrotic mechanisms in various cardiovascular disease models. This study investigated the role of miR-21 and miR-29b in a mouse model of AngII-induced arterial remodeling. Materials and methods Angiotensin II (AngII) (1000ng/kg/min) was infused via osmotic pumps in 10-week-old apoE-/- male mice (C57BL/6J background) for 7 days. Subsequently, arterial stiffness was determined in vivo using ultrasound-based measurements. Abdominal aortas were harvested and expression of various collagen isoforms (Col1a1, Col3a1, Col5a1) known to be crucial determinants of arterial remodeling/stiffening was quantified via qRT-PCR. We also measured expression levels of miR-21 and miR-29b. Results AngII stimulation resulted in an increased aortic stiffness paralleled by a marked pro-fibrotic response as evidenced by significant increases in Col1a1, Col3a1, and Col5a1 in the infrarenal aorta compared to baseline levels (p < 0.05). This increase was accompanied by significant downregulation of miR-29b, and upregulation of miR-21 (p <0.05). Conclusion The pro-fibrotic response in AngII-mediated arterial remodeling is associated with an increase in miR-21 and a decrease in miR-29b. Modulation of miR-21 and miR-29b have both been successful in altering fibrotic mechanisms in various cardiovascular diseases. These data suggest they may also be potential targets in the treatment of hypertensive vascular remodeling/arterial stiffening.

Autoregulation of blood flow in renal medulla of the rat: no role for angiotensin II

1988 ◽  
Vol 66 (6) ◽  
pp. 833-836 ◽  
Author(s):  
W. A. Cupples ◽  
D. J. Marsh
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Lower Limit ◽  
Enzyme Inhibitor ◽  
Renal Medulla ◽  
Converting Enzyme ◽  
Converting Enzyme Inhibitor ◽  
Upper Limit ◽  
Vasa Recta

Autoregulation of blood flow was assessed by a dual-slit technique in descending and ascending vasa recta of the exposed renal papillae of antidiuretic rats. There was complete autoregulation of blood flow in descending vasa recta. The lower limit of autoregulation was approximately 85 mmHg (1 mmHg = 133.3 Pa) and the upper limit was greater then 160 mmHg. Auto-regulation in ascending vasa recta was also good. To test the role of angiotensin II in this autoregulation, the converting enzyme inhibitor captopril was infused. Captopril had no effect on autoregulation of blood flow in either descending or ascending vasa recta. We conclude that blood flow in vasa recta of renal medulla is efficiently autoregulated and that this autoregulation is independent of angiotensin II

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