scholarly journals Changes in renin‐angiotensin‐aldosterone system during cardiac remodeling after mitral valvuloplasty in dogs

2022 ◽  
Author(s):  
Chieh‐Jen Cheng ◽  
Ahmed Mandour ◽  
Tomohiko Yoshida ◽  
Toshihiro Watari ◽  
Ryou Tanaka ◽  
...  
Keyword(s):  
Cardiac Remodeling ◽  
Renin Angiotensin Aldosterone System ◽  
Mitral Valvuloplasty ◽  
Renin Angiotensin

scholarly journals IMPACT OF TORSEMIDE ON CARDIAC REMODELING AND RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM IN HEART FAILURE PATIENTS

2020 ◽  
Vol 75 (11) ◽  
pp. 760
Author(s):  
Bishoy Abraham ◽  
Michael Megaly ◽  
Mina Sous ◽  
Boshra Louka ◽  
Robert Fraser ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiac Remodeling ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin ◽  
Heart Failure Patients

scholarly journals Mineralocorticoid Receptor Blockade Attenuates Chronic Overexpression of the Renin-Angiotensin-Aldosterone System Stimulation of Reduced Nicotinamide Adenine Dinucleotide Phosphate Oxidase and Cardiac Remodeling

Endocrinology ◽  
2007 ◽  
Vol 148 (8) ◽  
pp. 3773-3780 ◽  
Author(s):  
Sameer Stas ◽  
Adam Whaley-Connell ◽  
Javad Habibi ◽  
Lama Appesh ◽  
Melvin R. Hayden ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cardiac Remodeling ◽  
Nicotinamide Adenine Dinucleotide ◽  
Mineralocorticoid Receptor ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Resonance Imaging ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin ◽  
Transmission Electron ◽  
Reduced Nicotinamide Adenine Dinucleotide

The renin-angiotensin-aldosterone system contributes to cardiac remodeling, hypertrophy, and left ventricular dysfunction. Angiotensin II and aldosterone (corticosterone in rodents) together generate reactive oxygen species (ROS) via reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, which likely facilitate this hypertrophy and remodeling. This investigation sought to determine whether cardiac oxidative stress and cellular remodeling could be attenuated by in vivo mineralocorticoid receptor (MR) blockade in a rodent model of the chronically elevated tissue renin-angiotensin-aldosterone system, the transgenic TG (mRen2) 27 rat (Ren2). The Ren2 overexpresses the mouse renin transgene with resultant hypertension, insulin resistance, proteinuria, and cardiovascular damage. Young (6- to 7-wk-old) male Ren2 and age-matched Sprague-Dawley rats were treated with spironolactone or placebo for 3 wk. Heart tissue ROS, immunohistochemical analysis of 3-nitrotyrosine, and NADPH oxidase (NOX) subunits (gp91phox recently renamed NOX2, p22phox, Rac1, NOX1, and NOX4) were measured. Structural changes were assessed with cine-magnetic resonance imaging, transmission electron microscopy, and light microscopy. Significant increases in Ren2 septal wall thickness (cine-magnetic resonance imaging) were accompanied by perivascular fibrosis, increased mitochondria, and other ultrastructural changes visible by light microscopy and transmission electron microscopy. Although there was no significant reduction in systolic blood pressure, significant improvements were seen with MR blockade on ROS formation and NOX subunits (each P < 0.05). Collectively, these data suggest that MR blockade, independent of systolic blood pressure reduction, improves cardiac oxidative stress-induced structural and functional changes, which are driven, in part, by angiotensin type 1 receptor-mediated increases in NOX.

Brain renin–angiotensin–aldosterone system and ventricular remodeling after myocardial infarct: a reviewThis article is one of a selection of papers published in a special issue on Advances in Cardiovascular Research.

2009 ◽  
Vol 87 (12) ◽  
pp. 979-988 ◽  
Author(s):  
Katherine V. Westcott ◽  
Bing S. Huang ◽  
Frans H.H. Leenen
Keyword(s):  
Cardiac Remodeling ◽  
Cardiac Myocyte ◽  
Ventricular Remodeling ◽  
Myocardial Infarct ◽  
Cellular Level ◽  
Left Ventricular ◽  
Cardiovascular Research ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin ◽  
Cardiac Myocyte Apoptosis

After a myocardial infarct (MI), a variety of mechanisms contribute to progressive cardiac remodeling and dysfunction. Progressive activation of central sympathoexcitatory pathways appears to depend on a neuromodulatory pathway, involving local production of aldosterone and release of endogenous ouabain-like compounds (‘ouabain’) possibly from magnocellular neurons in the supraoptic and paraventricular nuclei. ‘Ouabain’ may lower the membrane potential of neurons and thereby enhance activity of angiotensinergic pathways. These central pathways appear to coordinate progressive activation of several peripheral mechanisms such as sympathetic tone and circulating and cardiac renin–angiotensin–aldosterone system (RAAS). Central blockade of aldosterone production, mineralocorticoid receptors, ‘ouabain’ activity, or AT1 receptors similarly prevents activation of these peripheral mechanisms. Cardiac remodeling after MI involves progressive left ventricular dilation, fibrosis, and decrease in contractile performance. Central blockade of this neuromodulatory pathway causes a marked attenuation of the remodeling and dysfunction, presumably by inhibiting increases in (cardiac) sympathetic activity and RAAS. At the cellular level, these systems may contribute to the cardiac remodeling by activating proinflammatory cytokines and cardiac myocyte apoptosis. New therapeutic approaches, specifically preventing activation of this brain neuromodulatory pathway, may lead to more optimal and specific approaches to the prevention of heart failure after MI.

EFFECTS OF PROGESTERONE AND OF FOUR SYNTHETIC GESTAGENS ON THE RENIN-ANGIOTENSIN-ALDOSTERONE-SYSTEM IN MAN.

1974 ◽  
Vol 77 (1_Suppl) ◽  
pp. S55
Author(s):  
W. Oelkers ◽  
M. Schöneshöfer ◽  
H. Blümel ◽  
H. Kutschke ◽  
H. Kreiser ◽  
...  
Keyword(s):  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin

NATRIURETIC PEPTIDES LEVEL AND THE STATUS OF THE RENIN – ANGIOTENSIN-ALDOSTERONE SYSTEM IN CHRONIC KIDNEY DISEASE IN PATIENTS WITH CONGENITAL MALFORMATIONS OF THE URINARY SYSTEM

2018 ◽  
Vol 22 (5) ◽  
pp. 45-50
Author(s):  
A. M. Mambetova ◽  
A. M. Inarokova ◽  
N. N. Shabalova ◽  
D. V. Bizheva ◽  
A. T. Mahiyeva
Keyword(s):  
Congenital Malformations ◽  
Control Group ◽  
Healthy Children ◽  
Urinary System ◽  
Renin Angiotensin Aldosterone System ◽  
Natriuretic Hormone ◽  
Renin Angiotensin ◽  
Group I ◽  
The Status ◽  
Sick Children

THE AIM. To determine the concentration of natriuretic peptide in the blood serum in children with congenital malformations of the urinary system (CM US) and to compare with the activity of renin-angiotensin-aldosterone system (RAAS).MATERIALS AND METHODS.119 patients with CM US aged 3 to 18 years were examined. A control group of 10 clinically healthy children. 3 groups were assigned: group I – 55 children with  congenital vesicoureteral reflux, and group II – 34 children with  congenital hydronephrosis and ureterohydronephrosis, III group – 30 children with other forms of dysembryogenesis of the US. Following indicators were identified by ELISA in the blood: renin, aldosterone,  N – terminal propeptide natriuretic hormone (NT-рroВNР). RESULTS.NT-рroВNР, renin and aldosterone hyperproduction were diagnosed in 59,6%, 69,7%, 54.6 % of sick children relatively. Concentrations were higher in all variants of  malformations in comparison with the control group. Significant  differences were revealed in obstructive species, where arterial  hypertension (AH) was diagnosed more often. Patients with AH  recorded significantly higher concentrations of NT-proВNР and renin.CONCLUSION.The key point in pathological processes developmentand progression in the cardiovascular system and kidneys is the  activation of RAAS. The system of natriuretic factors is important in maintaining the compensated state of patients due to the blockade of RAAS.

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