The Role of Angiotensin II AT1 Receptor in the Maintenance of Hemodynamics in a Canine Model of Coronary Microembolization-Induced Heart Failure

1999 ◽  
Vol 33 (2) ◽  
pp. 335-340 ◽  
Author(s):  
Jie Wang ◽  
Geng-Hua Yi ◽  
Shu-Ming Zhu ◽  
An-Guo Gu ◽  
Sulli Popilskis ◽  
...  
Keyword(s):  
Heart Failure ◽  
Angiotensin Ii ◽  
Canine Model ◽  
At1 Receptor ◽  
Coronary Microembolization

ACE2/Angiotensin-(1-7)/Mas Receptor Axis in Human Cancer: Potential Role for Pediatric Tumors

2020 ◽  
Vol 21 (9) ◽  
pp. 892-901 ◽  
Author(s):  
Ana Luiza Ataide Carneiro de Paula Gonzaga ◽  
Vitória Andrade Palmeira ◽  
Thomas Felipe Silva Ribeiro ◽  
Larissa Braga Costa ◽  
Karla Emília de Sá Rodrigues ◽  
...  
Keyword(s):  
Clinical Trials ◽  
Angiotensin Ii ◽  
Pediatric Cancer ◽  
Pediatric Patients ◽  
Human Cancer ◽  
Experimental Studies ◽  
At1 Receptor ◽  
Pediatric Tumors ◽  
Mas Receptor

Background: Pediatric tumors remain the highest cause of death in developed countries. Research on novel therapeutic strategies with lesser side effects is of utmost importance. In this scenario, the role of Renin-Angiotensin System (RAS) axes, the classical one formed by angiotensinconverting enzyme (ACE), Angiotensin II and AT1 receptor and the alternative axis composed by ACE2, Angiotensin-(1-7) and Mas receptor, have been investigated in cancer. Objective: This review aimed to summarize the pathophysiological role of RAS in cancer, evidence for anti-tumor effects of ACE2/Angiotensin-(1-7)/Mas receptor axis and future therapeutic perspectives for pediatric cancer. Methods: Pubmed, Scopus and Scielo were searched in regard to RAS molecules in human cancer and pediatric patients. The search terms were “RAS”, “ACE”, “Angiotensin-(1-7)”, “ACE2”, “Angiotensin II”, “AT1 receptor”, “Mas receptor”, “Pediatric”, “Cancer”. Results: Experimental studies have shown that Angiotensin-(1-7) inhibits the growth of tumor cells and reduces local inflammation and angiogenesis in several types of cancer. Clinical trials with Angiotensin-( 1-7) or TXA127, a pharmaceutical grade formulation of the naturally occurring peptide, have reported promising findings, but not enough to recommend medical use in human cancer. In regard to pediatric cancer, only three articles that marginally investigated RAS components were found and none of them evaluated molecules of the alternative RAS axis. Conclusion: Despite the potential applicability of Angiotensin-(1-7) in pediatric tumors, the role of this molecule was never tested. Further clinical trials are necessary, also including pediatric patients, to confirm safety and efficiency and to define therapeutic targets.

scholarly journals Role of angiotensin II in the altered renal function of congestive heart failure.

1984 ◽  
Vol 55 (5) ◽  
pp. 669-675 ◽  
Author(s):  
I Ichikawa ◽  
J M Pfeffer ◽  
M A Pfeffer ◽  
T H Hostetter ◽  
B M Brenner
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Renal Function ◽  
Angiotensin Ii

scholarly journals Role of Oxidant Stress on AT1 Receptor Expression in Neurons of Rabbits With Heart Failure and in Cultured Neurons

2008 ◽  
Vol 103 (2) ◽  
pp. 186-193 ◽  
Author(s):  
Dongmei Liu ◽  
Lie Gao ◽  
Shyamal K. Roy ◽  
Kurtis G. Cornish ◽  
Irving H. Zucker
Keyword(s):  
Heart Failure ◽  
Oxidant Stress ◽  
At1 Receptor ◽  
Receptor Expression ◽  
Cultured Neurons

Role of Angiotensin II AT1 Receptor Blockers in the Treatment of Arterial Hypertension

2003 ◽  
Vol 10 (6) ◽  
pp. 401-408 ◽  
Author(s):  
Freddy Contreras ◽  
Mar??a Antonia de la Parte ◽  
Julio Cabrera ◽  
Nestor Ospino ◽  
Zafar H. Israili ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Arterial Hypertension ◽  
At1 Receptor ◽  
Receptor Blockers ◽  
At1 Receptor Blockers

scholarly journals A REVIEW ON COMPARATIVE STUDY ON THE SAFETY AND EFFECTIVENESS OF SACUBITRIL-VALSARTAN COMBINATION WITH ACE/ARB THERAPY IN CARDIAC PATIENTS

2019 ◽  
Vol 7 (2) ◽  
Author(s):  
Bhagya Suresh ◽  
Mathew George ◽  
Lincy Joseph
Keyword(s):  
Heart Failure ◽  
Angiotensin Ii ◽  
Angiotensin Converting Enzyme ◽  
Left Ventricular ◽  
At1 Receptor ◽  
Receptor Blocker ◽  
Left Ventricular Ejection ◽  
Ang Ii ◽  
Converting Enzyme ◽  
Cv Disease

Cardiovascular (CV) disease is a major cause of morbidity and mortality in the developing and the developed world, and represents a major barrier to sustainable human development. Ischemic heart disease, cerebrovascular disease, cardiomyopathy and heart failure (HF), and hypertension among others represent major forms of CV disease. Heart failure (HF) is among the key contributors to the CV-related health care burden, a uninterrupted concern despite the utilization of clinically tried guideline-directed therapies. The most common cause for HF is reduced left cavum heart muscle perform. ARBs produce equivalent mortality benefits with fewer adverse effects than ACE inhibitors. Angiotensin converting enzyme (ACEI) reduces the combined risk of death or hospitalization, slow progression of HF, and reduced rate of reinfarction. Sacubitril/valsartan could be a first-in-class twin action molecule of the neprilysin (NEP) substance sacubitril (AHU-377) and therefore the angiotensin II (Ang II) sort one (AT1) receptor blocker (ARB) valsartan. The beneficial antihypertensive and HF effects of sacubitril/valsartan are mediated through the inhibition of NEP in catabolizing the natriuretic peptides (NPs) and the blockade of Ang II, AT1 receptor with valsartan. These actions of sacubitril/ valsartan end in general dilation and inflated symptoms and symptoms, resulting in decrease in peripheral tube resistance and plasma volume contraction, all necessary actions for the lowering of BP and improving HF symptoms. Keywords:  cardiovascular disease, left ventricular ejection fraction, angiotensin II receptor blocker, angiotensin converting enzyme, sacubitril/valsartan.

scholarly journals Stearoyl-CoA Desaturase (SCD) Induces Cardiac Dysfunction with Cardiac Lipid Overload and Angiotensin II AT1 Receptor Protein Up-Regulation

2021 ◽  
Vol 22 (18) ◽  
pp. 9883
Author(s):  
Joshua Abd Alla ◽  
Yahya F. Jamous ◽  
Ursula Quitterer
Keyword(s):  
Heart Failure ◽  
Angiotensin Ii ◽  
Cardiac Dysfunction ◽  
Fatty Acid Synthase ◽  
Left Ventricular ◽  
At1 Receptor ◽  
Receptor Protein ◽  
Cardiac Lipid ◽  
Stearoyl Coa Desaturase ◽  
The Impact

Heart failure is a major cause of death worldwide with insufficient treatment options. In the search for pathomechanisms, we found up-regulation of an enzyme, stearoyl-CoA desaturase 1 (Scd1), in different experimental models of heart failure induced by advanced atherosclerosis, chronic pressure overload, and/or volume overload. Because the pathophysiological role of Scd1/SCD in heart failure is not clear, we investigated the impact of cardiac SCD upregulation through the generation of C57BL/6-Tg(MHCSCD)Sjaa mice with myocardium-specific expression of SCD. Echocardiographic examination showed that 4.9-fold-increased SCD levels triggered cardiac hypertrophy and symptoms of heart failure at an age of eight months. Tg-SCD mice had a significantly reduced left ventricular cardiac ejection fraction of 25.7 ± 2.9% compared to 54.3 ± 4.5% of non-transgenic B6 control mice. Whole-genome gene expression profiling identified up-regulated heart-failure-related genes such as resistin, adiponectin, and fatty acid synthase, and type 1 and 3 collagens. Tg-SCD mice were characterized by cardiac lipid accumulation with 1.6- and 1.7-fold-increased cardiac contents of saturated lipids, palmitate, and stearate, respectively. In contrast, unsaturated lipids were not changed. Together with saturated lipids, apoptosis-enhancing p53 protein contents were elevated. Imaging by autoradiography revealed that the heart-failure-promoting and membrane-spanning angiotensin II AT1 receptor protein of Tg-SCD hearts was significantly up-regulated. In transfected HEK cells, the expression of SCD increased the number of cell-surface angiotensin II AT1 receptor binding sites. In addition, increased AT1 receptor protein levels were detected by fluorescence spectroscopy of fluorescent protein-labeled AT1 receptor-Cerulean. Taken together, we found that SCD promotes cardiac dysfunction with overload of cardiotoxic saturated lipids and up-regulation of the heart-failure-promoting AT1 receptor protein.

High-output heart failure in the dog: systemic and intrarenal role of angiotensin II

1975 ◽  
Vol 229 (2) ◽  
pp. 474-478 ◽  
Author(s):  
RH Freeman ◽  
JO Davis ◽  
WS Spielman ◽  
TE Lohmeier
Keyword(s):  
Heart Failure ◽  
Blood Flow ◽  
Angiotensin Ii ◽  
Arterial Infusion ◽  
Additional Information ◽  
High Output Heart Failure ◽  
Anesthetized Dogs ◽  
The Mean ◽  
High Output

Dogs with experimental high-output heart failure (HOF) exhibit marked retention of salt and water secondary to hypersecretion of both renin and aldosterone. The present study was undertaken to evaluate the systemic and intrarenal arteriolar action of angiotensin II (AII) in dogs with HOF and to provide additional information about the role of AII in low-output states. The intravenous infusion of a specific AII antagonist, [Sar1, Ala8]AII (6 mug/kg min-1), into conscious dogs with HOF decreased the mean arterial pressure (AP) from 101 +/- 7 to 83 +/- 7 mmHg (P less than 0.01) after 45 min of infusion. Intrarenal arterial infusion of the AII antagonist (0.2 and 2.0 mug/kg min-1) into anesthetized dogs with HOF also decreased AP and produced a marked increase in renal blood flow (RBF) with no changes in either creatinine clearance or sodium excretion. Similar results were obtained during the intrarenal infusion of the antagonist into sodium-depleted dogs and dogs with thoracic vena caval constriction, but not in normal dogs. The data demonstrate an important role for AII in the regulation of AP and RBF in high- and low-output states.

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