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Journal articles on the topic 'Angiotensin II (AngII)'

Author: Grafiati

Published: 4 June 2021

Last updated: 10 February 2022

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1

Kohler, Konrad, Thomas Wheeler-Schilling, Bernhard Jurklies, Elke Guenther, and Eberhart Zrenner. "Angiotensin II in the rabbit retina." Visual Neuroscience 14, no. 1 (1997): 63–71. http://dx.doi.org/10.1017/s0952523800008762.

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AbstractWe investigated a putative local angiotensin II (AngII) system in the rabbit retina by examining AngII contents in the retina, vitreous humor, and choroid by radioimmunoassays and AngII synthesis in the retina and choroid by detection of angiotensin converting enzyme (ACE) mRNA. An antibody directed against AngII was used to localize possible cellular sources of AngII in the retina. To enhance immunoreactivity and to further examine AngII metabolism, tissues were preincubated in medium containing either protease inhibitors (PI), PI together with the AngII-precursor AngI, or PI and AngI

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Bosnyak, Sanja, Emma S. Jones, Arthur Christopoulos, Marie-Isabel Aguilar, Walter G. Thomas, and Robert E. Widdop. "Relative affinity of angiotensin peptides and novel ligands at AT1 and AT2 receptors." Clinical Science 121, no. 7 (2011): 297–303. http://dx.doi.org/10.1042/cs20110036.

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AT1R (angiotensin type 1 receptor) and AT2R (angiotensin type 2 receptor) are well known to be involved in the complex cardiovascular actions of AngII (angiotensin II). However, shorter peptide fragments of AngII are thought to have biological activity in their own right and elicit effects that oppose those mediated by AngII. In the present study, we have used HEK (human embryonic kidney)-293 cells stably transfected with either AT1R or AT2R to perform a systematic analysis of binding affinities of all the major angiotensin peptides. Additionally, we tested the novel AT2R agonist Compound 21,

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HILL-KAPTURCZAK, NATHALIE, MATTHIAS H. KAPTURCZAK, EDWARD R. BLOCK, et al. "Angiotensin II-Stimulated Nitric Oxide Release from Porcine Pulmonary Endothelium Is Mediated by Angiotensin IV." Journal of the American Society of Nephrology 10, no. 3 (1999): 481–91. http://dx.doi.org/10.1681/asn.v103481.

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Abstract. In this study, a nitric oxide (NO) sensor was used to examine the ability of angiotensin II (AngII), AngIV, and bradykinin (Bk) to stimulate NO release from porcine pulmonary artery (PPAE) and porcine aortic endothelial (PAE) cells and to explore the mechanism of the AngII-stimulated NO release. Physiologic concentrations of AngII, but not Bk, caused release of NO from PPAE cells. In contrast, Bk, but not AngII, stimulated NO release from PAE cells. AngII-stimulated NO release from PPAE cells required extracellular L-arginine and was inhibited by L-nitro-arginine methyl ester. AT1 an

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4

Yamaguchi, Nobuharu, Daniel Martineau, Stéphane Lamouche, and Richard Briand. "Functional role of local angiotensin-converting enzyme (ACE) in adrenal catecholamine secretion in vivo." Canadian Journal of Physiology and Pharmacology 77, no. 11 (1999): 878–85. http://dx.doi.org/10.1139/y99-094.

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The aim of the present study was to investigate whether exogenous angiotensin I (AngI) is locally converted to angiotensin II (AngII), which in turn results in an increase in the adrenal catecholamine (CA) secretion in the adrenal gland in anesthetized dogs. Plasma CA concentrations in adrenal venous and aortic blood were determined by an HPLC-electrochemical method. Adrenal venous blood flow was measured by gravimetry. Local administration of AngI (0.0062 to 6.2 µg, 0.0096 to 9.6 µM) to the left adrenal gland resulted in significant increases in CA output in a dose-dependent manner. Following

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KOBORI, HIROYUKI, LISA M. HARRISON-BERNARD, and L. GABRIEL NAVAR. "Expression of Angiotensinogen mRNA and Protein in Angiotensin II-Dependent Hypertension." Journal of the American Society of Nephrology 12, no. 3 (2001): 431–39. http://dx.doi.org/10.1681/asn.v123431.

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Abstract. Chronic elevations in circulating angiotensin II (AngII) levels produce sustained hypertension and increased intrarenal AngII contents through multiple mechanisms, which may include sustained or increased local production of AngII. This study was designed to test the hypothesis that chronic AngII infusion increases renal angiotensinogen mRNA and protein levels, thus contributing to the increase in intrarenal AngII levels. AngII (80 ng/min) was infused subcutaneously for 13 d into Sprague-Dawley rats, using osmotic minipumps. Control rats underwent sham operations. By day 12, systolic

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Horiuchi, Masatsugu, Jun Iwanami, and Masaki Mogi. "Regulation of angiotensin II receptors beyond the classical pathway." Clinical Science 123, no. 4 (2012): 193–203. http://dx.doi.org/10.1042/cs20110677.

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The RAS (renin–angiotensin system) plays a role not only in the cardiovascular system, including blood pressure regulation, but also in the central nervous system. AngII (angiotensin II) binds two major receptors: the AT1 receptor (AngII type 1 receptor) and AT2 receptor (AngII type 2 receptor). It has been recognized that AT2 receptor activation not only opposes AT1 receptor actions, but also has unique effects beyond inhibitory cross-talk with AT1 receptor signalling. Novel pathways beyond the classical actions of RAS, the ACE (angiotensin-converting enzyme)/AngII/AT1 receptor axis, have bee

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7

Zhou, Yi, Xiaoxu Guan, Xiaoyi Chen, et al. "Angiotensin II/Angiotensin II Receptor Blockade Affects Osteoporosis via the AT1/AT2-Mediated cAMP-Dependent PKA Pathway." Cells Tissues Organs 204, no. 1 (2017): 25–37. http://dx.doi.org/10.1159/000464461.

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Animal studies have reported on the benefits of ARB on bone mass. However, the underlying mechanism for angiotensin II (AngII)/AngII receptor blockade (ARB) in regulating bone mass remains elusive. Since high levels of plasma and urine cAMP are observed in osteoporotic and hypertensive patients, we hypothesized that cAMP may be an important molecule for the downstream events of the activation of AT receptors, members of the G-protein-coupled receptor family, in regulating bone turnover. In this study, micro-CT and X-ray analyses indicated that AngII decreased bone mass via biasing bone resorpt

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Laporte, Stéphane A., Antony A. Boucard, Guy Servant, Gaétan Guillemette, Richard Leduc, and Emanuel Escher. "Determination of Peptide Contact Points in the Human Angiotensin II Type I Receptor (AT1) with Photosensitive Analogs of Angiotensin II." Molecular Endocrinology 13, no. 4 (1999): 578–86. http://dx.doi.org/10.1210/mend.13.4.0270.

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Abstract To identify ligand-binding domains of Angiotensin II (AngII) type 1 receptor (AT1), two different radiolabeled photoreactive AngII analogs were prepared by replacing either the first or the last amino acid of the octapeptide by p-benzoyl-l-phenylalanine (Bpa). High yield, specific labeling of the AT1 receptor was obtained with the 125I-[Sar1,Bpa8]AngII analog. Digestion of the covalent 125I-[Sar1,Bpa8]AngII-AT1 complex with V8 protease generated two major fragments of 15.8 kDa and 17.8 kDa, as determined by SDS-PAGE. Treatment of the[ Sar1,Bpa8]AngII-AT1 complex with cyanogen bromide

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Jang, Hee-Seong, Jee In Kim, Jinu Kim, Jeen-Woo Park, and Kwon Moo Park. "Angiotensin II Removes Kidney Resistance Conferred by Ischemic Preconditioning." BioMed Research International 2014 (2014): 1–10. http://dx.doi.org/10.1155/2014/602149.

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Ischemic preconditioning (IPC) by ischemia/reperfusion (I/R) renders resistance to the kidney. Strong IPC triggers kidney fibrosis, which is involved in angiotensin II (AngII) and its type 1 receptor (AT1R) signaling. Here, we investigated the role of AngII/AT1R signal pathway in the resistance of IPC kidneys to subsequent I/R injury. IPC of kidneys was generated by 30 minutes of bilateral renal ischemia and 8 days of reperfusion. Sham-operation was performed to generate control (non-IPC) mice. To examine the roles of AngII and AT1R in IPC kidneys to subsequent I/R, IPC kidneys were subjected

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Binz-Lotter, Julia, Christian Jüngst, Markus M. Rinschen, et al. "Injured Podocytes Are Sensitized to Angiotensin II–Induced Calcium Signaling." Journal of the American Society of Nephrology 31, no. 3 (2020): 532–42. http://dx.doi.org/10.1681/asn.2019020109.

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BackgroundInhibition of angiotensin II (AngII) signaling, a therapeutic mainstay of glomerular kidney diseases, is thought to act primarily through regulating glomerular blood flow and reducing filtration pressure. Although extravascular actions of AngII have been suggested, a direct effect of AngII on podocytes has not been demonstrated in vivo.MethodsTo study the effects of AngII on podocyte calcium levels in vivo, we used intravital microscopy of the kidney in mice expressing the calcium indicator protein GCaMP3.ResultsIn healthy animals, podocytes displayed limited responsiveness to AngII

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Hondrelis, John, John Matsoukas, George Agelis, et al. "1H NMR Conformational Studies in Water of Angiotensin II Analogues Modified at the N- and C-Termini: Interactions of the Aromatic Side Chains and Folding of the N-Terminal Domain." Collection of Czechoslovak Chemical Communications 59, no. 11 (1994): 2523–32. http://dx.doi.org/10.1135/cccc19942523.

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The conformation of [Sar1]angiotensin II in water at neutral pH has been examined by proton magnetic resonance spectroscopy at 400 MHz and in particular by comparing its 1H NMR spectral data with those of analogues modified at positions 1,4 and 6, namely [Sar1,Cha8]ANGII, [Des Asp1,Cha8]ANGII, [Aib1,Tyr(Me)4]ANGII, [Aib1,Tyr(Me)4,Ile8]ANGII, [N-MeAib1,Tyr(Me)4]ANGII, [N-MeAib1,Tyr(Me)4,Ile8]ANGII, ANGIII and [Sar1,Ile8]ANGII. Assignment of all proton resonances in these analogues was made possible by 2D COSY NMR experiments. The H-2 and H-4 protons for the histidine ring in [Sar1]ANGII, ANGII

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Ferreira, Rogério, Bernardo Gasperin, Monique Rovani, et al. "Angiotensin II Signaling Promotes Follicle Growth and Dominance in Cattle." Endocrinology 152, no. 12 (2011): 4957–65. http://dx.doi.org/10.1210/en.2011-1146.

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It is generally understood that angiotensin II (AngII) promotes follicle atresia in rats, although recent data suggested that this may not be true in cattle. In this study, we aimed to determine in vivo whether AngII alters follicle development in cattle, using intrafollicular injection of AngII or antagonist into the growing dominant follicle or the second largest subordinate follicle. Injection of saralasin, an AngII antagonist, into the growing dominant follicle inhibited follicular growth, and this inhibitory effect was overcome by systemic FSH supplementation. Injection of AngII into the

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Surapongchai, Juthamard, Mujalin Prasannarong, Tepmanas Bupha-Intr, and Vitoon Saengsirisuwan. "Angiotensin II induces differential insulin action in rat skeletal muscle." Journal of Endocrinology 232, no. 3 (2017): 547–60. http://dx.doi.org/10.1530/joe-16-0579.

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Angiotensin II (ANGII) is reportedly involved in the development of skeletal muscle insulin resistance. The present investigation evaluated the effects of two ANGII doses on the phenotypic characteristics of insulin resistance syndrome and insulin action and signaling in rat skeletal muscle. Male Sprague–Dawley rats were infused with either saline (SHAM) or ANGII at a commonly used pressor dose (100 ng/kg/min; ANGII-100) or a higher pressor dose (500 ng/kg/min; ANGII-500) via osmotic minipumps for 14 days. We demonstrated that ANGII-100-infused rats exhibited the phenotypic features of non-obe

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Reaux, A., X. Iturrioz, G. Vazeux, et al. "Aminopeptidase A, which generates one of the main effector peptides of the brain renin-angiotensin system, angiotensin III, has a key role in central control of arterial blood pressure." Biochemical Society Transactions 28, no. 4 (2000): 435–40. http://dx.doi.org/10.1042/bst0280435.

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Overactivity of the brain renin-angiotensin system (RAS) has been implicated in the development and maintenance of hypertension in several experimental animal models. We have recently reported that, in the murine brain RAS, angiotensin II (AngII) is converted by aminopeptidase A (APA) into angiotensin III (AngIII), which is itself degraded by aminopeptidase N (APN), both peptides being equipotent to increase vasopressin release and arterial blood pressure when injected by the intracerebroventricular (i.c.v.) route. Because AngII is converted in vivo into AngIII, the exact nature of the active

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Hirohama, Daigoro, Nobuhiro Ayuzawa, Kohei Ueda, et al. "Aldosterone Is Essential for Angiotensin II-Induced Upregulation of Pendrin." Journal of the American Society of Nephrology 29, no. 1 (2017): 57–68. http://dx.doi.org/10.1681/asn.2017030243.

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The renin-angiotensin-aldosterone system has an important role in the control of fluid homeostasis and BP during volume depletion. Dietary salt restriction elevates circulating angiotensin II (AngII) and aldosterone levels, increasing levels of the Cl−/HCO3− exchanger pendrin in β-intercalated cells and the Na+-Cl− cotransporter (NCC) in distal convoluted tubules. However, the independent roles of AngII and aldosterone in regulating these levels remain unclear. In C57BL/6J mice receiving a low-salt diet or AngII infusion, we evaluated the membrane protein abundance of pendrin and NCC; assessed

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Pavo, Noemi, Georg Goliasch, Raphael Wurm, et al. "Low- and High-renin Heart Failure Phenotypes with Clinical Implications." Clinical Chemistry 64, no. 3 (2018): 597–608. http://dx.doi.org/10.1373/clinchem.2017.278705.

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Abstract BACKGROUND Blockade of the renin–angiotensin system (RAS) represents a main strategy in the therapy of heart failure with reduced ejection fraction (HFrEF), but the role of active renin concentration (ARC) for guiding therapy in the presence of an RAS blockade remains to be established. This study assessed angiotensin profiles of HFrEF patients with distinct RAS activations as reflected by ARC. METHODS Two cohorts of stable chronic HFrEF patients on optimal medical treatment (OMT) were enrolled. We assessed ARC and all known circulating angiotensin metabolites, including AngI and AngI

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Chipitsyna, Galina, Qiaoke Gong, Chance F. Gray, Yasir Haroon, Erdinc Kamer та Hwyda A. Arafat. "Induction of Monocyte Chemoattractant Protein-1 Expression by Angiotensin II in the Pancreatic Islets and β-Cells". Endocrinology 148, № 5 (2007): 2198–208. http://dx.doi.org/10.1210/en.2006-1358.

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Angiotensin II (AngII), the principal hormone of the renin-angiotensin system, is actively generated in the pancreas and has been suggested as a key mediator of inflammation. Monocyte chemoattractant protein-1 (MCP-1) is a chemokine that plays an important role in the recruitment of mononuclear cells into the pancreatic islets. In this study, we investigated the potential molecular basis for the role of AngII in islet inflammation through studying its effect on MCP-1. AngII significantly increased the expression of MCP-1 mRNA and protein in the RINm5F β-cell line and activated MCP-1 promoter.

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Almeida-Pereira, G., T. Vilhena-Franco, R. Coletti та ін. "17β-Estradiol attenuates p38MAPK activity but not PKCα induced by angiotensin II in the brain". Journal of Endocrinology 240, № 2 (2019): 345–60. http://dx.doi.org/10.1530/joe-18-0095.

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17β-Estradiol (E2) has been shown to modulate the renin–angiotensin system in hydromineral and blood pressure homeostasis mainly by attenuating angiotensin II (ANGII) actions. However, the cellular mechanisms of the interaction between E2 and angiotensin II (ANGII) and its physiological role are largely unknown. The present experiments were performed to better understand the interaction between ANGII and E2 in body fluid control in female ovariectomized (OVX) rats. The present results are the first to demonstrate that PKC/p38 MAPK signaling is involved in ANGII-induced water and sodium intake

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GRUDEN, GABRIELLA, STEPHEN THOMAS, DAVINA BURT, et al. "Interaction of Angiotensin II and Mechanical Stretch on Vascular Endothelial Growth Factor Production by Human Mesangial Cells." Journal of the American Society of Nephrology 10, no. 4 (1999): 730–37. http://dx.doi.org/10.1681/asn.v104730.

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Abstract. The antiproteinuric effect of angiotensin-converting enzyme inhibitors underscores the importance of a hemodynamic injury and the renin-angiotensin system in the proteinuria of various glomerular diseases. Vascular endothelial growth factor (VEGF), a potent promoter of vascular permeability, is induced in mesangial cells by both mechanical stretch and TGF-β1. This study investigates the effect of TGF-β blockade, angiotensin II (AngII), and the interaction between AngII and stretch on human mesangial cell VEGF production. Exposure to AngII (1 μM) induced a significant increase in VEGF

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Zahradka, Peter, Brenda Litchie, Ben Storie, and Gail Helwer. "Transactivation of the Insulin-Like Growth Factor-I Receptor by Angiotensin II Mediates Downstream Signaling from the Angiotensin II Type 1 Receptor to Phosphatidylinositol 3-Kinase." Endocrinology 145, no. 6 (2004): 2978–87. http://dx.doi.org/10.1210/en.2004-0029.

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Abstract Angiotensin II (AngII) activates phosphatidylinositol 3-kinase (PI3-kinase), a known effector of receptor tyrosine kinases. Treatment of smooth muscle cells with AngII has also been shown to promote phosphorylation of various tyrosine kinase receptors. We therefore investigated the relationship between AngII and IGF-I receptor activation in smooth muscle cells with a phosphorylation-specific antibody. Our experiments showed that IGF-I receptor phosphorylation was maximally stimulated within 10 min by AngII. Inclusion of an IGF-I-neutralizing antibody in the culture media did not preve

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Moriyama, T., M. Fujibayashi, Y. Fujiwara, et al. "Angiotensin II stimulates interleukin-6 release from cultured mouse mesangial cells." Journal of the American Society of Nephrology 6, no. 1 (1995): 95–101. http://dx.doi.org/10.1681/asn.v6195.

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Interleukin-6 (IL-6) is a multifunctional cytokine exerting a wide variety of biologic responses, including cell proliferation. Recently, IL-6 has been known to play a role in the pathogenesis of mesangial proliferative glomerulonephritis. IL-6 is now recognized as an autocrine growth factor for glomerular mesangial cells, and various inflammatory mediators have been shown to promote IL-6 release from mesangial cells. However, little is known about the noninflammatory stimuli of IL-6 release from mesangial cells. In this study, it was hypothesized that angiotensin II (AngII) is one of the noni

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Fuentes, J., and F. B. Eddy. "Cardiovascular responses in vivo to angiotensin II and the peptide antagonist saralasin in rainbow trout Oncorhynchus mykiss." Journal of Experimental Biology 201, no. 2 (1998): 267–72. http://dx.doi.org/10.1242/jeb.201.2.267.

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The effects of [Asn1,Val5]-angiotensin II (AngII) and [Sar1,Val5, Ala8]-angiotensin II (saralasin) on dorsal aortic blood pressure, pulse pressure and heart rate were examined in rainbow trout in vivo. AngII when administered as a single dose of 25 microg kg-1 induced a biphasic response in blood pressure, with a significant hypertensive response during the initial 10 min, followed by a significant hypotension of 70-75 % compared with the initial blood pressure after 50 min and continuing until approximately 80 min post-injection. The co-administration of AngII (25 microg kg-1) and saralasin (

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Garbieri, Thais Francini, Victor Martin, Carlos Ferreira Santos, Pedro de Sousa Gomes, and Maria Helena Fernandes. "The Embryonic Chick Femur Organotypic Model as a Tool to Analyze the Angiotensin II Axis on Bone Tissue." Pharmaceuticals 14, no. 5 (2021): 469. http://dx.doi.org/10.3390/ph14050469.

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Activation of renin–angiotensin system (RAS) plays a role in bone deterioration associated with bone metabolic disorders, via increased Angiotensin II (AngII) targeting Angiotensin II type 1 receptor/Angiotensin II type 2 receptor (AT1R/AT2R). Despite the wide data availability, the RAS role remains controversial. This study analyzes the feasibility of using the embryonic chick femur organotypic model to address AngII/AT1R/AT2R axis in bone, which is an application not yet considered. Embryonic day-11 femurs were cultured ex vivo for 11 days in three settings: basal conditions, exposure to Ang

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Barrett-O’Keefe, Zachary, Melissa A. H. Witman, John Mcdaniel та ін. "Angiotensin II potentiates α-adrenergic vasoconstriction in the elderly". Clinical Science 124, № 6 (2012): 413–22. http://dx.doi.org/10.1042/cs20120424.

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Aging is characterized by increased sympatho-excitation, expressed through both the α-adrenergic and RAAS (renin–angiotensin–aldosterone) pathways. Although the independent contribution of these two pathways to elevated vasoconstriction with age may be substantial, significant cross-talk exists that could produce potentiating effects. To examine this interaction, 14 subjects (n=8 young, n=6 old) underwent brachial artery catheterization for administration of AngII (angiotensin II; 0.8–25.6 ng/dl per min), NE [noradrenaline (norepinephrine); 2.5–80 ng/dl per min] and AngII with concomitant α-ad

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Lorenzo, Óscar, Marta Ruiz-Ortega, Yusuke Suzuki та ін. "Angiotensin III Activates Nuclear Transcription Factor-κB in Cultured Mesangial Cells Mainly via AT2Receptors: Studies with AT1Receptor-Knockout Mice". Journal of the American Society of Nephrology 13, № 5 (2002): 1162–71. http://dx.doi.org/10.1681/asn.v1351162.

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ABSTRACT. Nuclear factor-κB (NF-κB) regulates many genes involved in renal pathophysiologic processes. It was previously demonstrated that angiotensin II (AngII) and its amino-terminal degradation product AngIII activate NF-κB in mesangial cells. However, which are the Ang receptor subtypes involved in the NF-κB pathway and whether these Ang peptides act through the same or different receptors in mesangial cells have not been evaluated. Under the culture conditions used, quiescent rat mesangial cells expressed both AT1and AT2receptors. To investigate the receptors involved in the NF-κB pathway

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Sykes, S. D., E. R. Lumbers, K. G. Pringle, T. Zakar, G. A. Dekker, and C. T. Roberts. "161. PREDICTING GESTATIONAL HYPERTENSION AND PREECLAMPSIA FROM MATERNAL ANGIOTENSIN II AND ANGIOTENSIN 1–7 LEVELS AT 15 WEEKS GESTATION." Reproduction, Fertility and Development 22, no. 9 (2010): 79. http://dx.doi.org/10.1071/srb10abs161.

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Angiotensin II (AngII) is the main effector peptide of the renin angiotensin system (RAS). The RAS is also involved in the aetiology of hypertension. Angiotensin 1–7 (Ang1–7) acting on the Mas receptor may counteract AngII effects. RAS activity is increased in early gestation. We wanted to determine if maternal plasma AngII and Ang1–7 levels in early gestation predict the onset of hypertension in late gestation. Circulating AngII and Ang1–7 have been measured by RIA (D Casley, Prosearch Pty. Ltd.) in EDTA treated plasma from healthy nulliparous pregnant women at 15 weeks gestation from the Ade

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Lu, Qing, Ana P. Davel, Adam P. McGraw, Sitara P. Rao, Brenna G. Newfell та Iris Z. Jaffe. "PKCδ Mediates Mineralocorticoid Receptor Activation by Angiotensin II to Modulate Smooth Muscle Cell Function". Endocrinology 160, № 9 (2019): 2101–14. http://dx.doi.org/10.1210/en.2019-00258.

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Abstract Angiotensin II (AngII) and the mineralocorticoid receptor (MR) ligand aldosterone both contribute to cardiovascular disorders, including hypertension and adverse vascular remodeling. We previously demonstrated that AngII activates MR-mediated gene transcription in human vascular smooth muscle cells (SMCs), yet the mechanism and the impact on SMC function are unknown. Using an MR-responsive element-driven transcriptional reporter assay, we confirm that AngII induces MR transcriptional activity in vascular SMCs and endothelial cells, but not in Cos1 or human embryonic kidney-293 cells.

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Wellman, Kimberly, Rui Fu, Amber Baldwin, Kent Riemondy, and Neelanjan Mukherjee. "RNA Decay Controls the Kinetics of the Angiotensin II Gene Expression Response." Journal of the Endocrine Society 5, Supplement_1 (2021): A508—A509. http://dx.doi.org/10.1210/jendso/bvab048.1040.

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Abstract Complex cellular resonses require the temporal coordination of stimulus-induced gene expression programs. Angiotensin II (AngII) is the active 8 amino acid peptide in the renin-angiotensin-aldosterone system that controls blood pressure and fluid balance. AngII binds to type I angiotensin receptor in the adrenal cortex to initiate a cascade of temporally coordinated events leading to the production of aldosterone, a master regulator of blood pressure and volume. We stimulated a steroidogenic human cell line (H295R) with AngII and performed RNA-seq at twelve points. We identified twelv

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Souza, Heraldo P., Denise Frediani, Ana L. Cobra, et al. "Angiotensin II modulates CD40 expression in vascular smooth muscle cells." Clinical Science 116, no. 5 (2009): 423–31. http://dx.doi.org/10.1042/cs20080155.

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The signalling pathway CD40/CD40L (CD40 ligand) plays an important role in atherosclerotic plaque formation and rupture. AngII (angiotensin II), which induces oxidative stress and inflammation, is also implicated in the progression of atherosclerosis. In the present study, we tested the hypothesis that AngII increases CD40/CD40L activity in vascular cells and that ROS (reactive oxygen species) are part of the signalling cascade that controls CD40/CD40L expression. Human CASMCs (coronary artery smooth muscle cells) in culture exposed to IL (interleukin)-1β or TNF-α (tumour necrosis factor-α) ha

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Torsoni, MA, JB Carvalheira, VC Calegari, et al. "Angiotensin II (AngII) induces the expression of suppressor of cytokine signaling (SOCS)-3 in rat hypothalamus - a mechanism for desensitization of AngII signaling." Journal of Endocrinology 181, no. 1 (2004): 117–28. http://dx.doi.org/10.1677/joe.0.1810117.

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Angiotensin II exerts a potent dypsogenic stimulus on the hypothalamus, which contributes to its centrally mediated participation in the control of water balance and blood pressure. Repetitive intracerebroventricular (i.c.v.) injections of angiotensin II lead to a loss of effect characterized as physiological desensitization to the peptide's action. In the present study, we demonstrate that angiotensin II induces the expression of suppressor of cytokine signaling (SOCS)-3 via angiotensin receptor 1 (AT1) and JAK-2, mostly located at the median preoptic lateral and anterodorsal preoptic nuclei.

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Fan, L., D. Javeshghani, S. Mukaddam-Daher, et al. "Effects of angiotensin II on plasma atrial natriuretic factor in nonpregnant and pregnant ewes." Canadian Journal of Physiology and Pharmacology 73, no. 5 (1995): 644–50. http://dx.doi.org/10.1139/y95-082.

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The release of atrial natriuretic factor (ANF) is primarily determined by atrial stretch, but may also be modulated by circulating angiotensin II (AngII). During pregnancy, the circulating concentrations of both ANF and AngII are increased. To further define possible effects of AngII on ANF release, four doses of AngII (0.5, 5, 20, 40 ng∙kg−1∙min−1) were intravenously infused into five nonpregnant and five pregnant (105–140 days of gestation) ewes alone and during the simultaneous infusion of sodium nitroprusside at doses sufficient to abolish the pressor effects of AngII. Mean arterial pressu

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Higuchi, Sadaharu, Haruhiko Ohtsu, Hiroyuki Suzuki, Heigoro Shirai, Gerald D. Frank, and Satoru Eguchi. "Angiotensin II signal transduction through the AT1 receptor: novel insights into mechanisms and pathophysiology." Clinical Science 112, no. 8 (2007): 417–28. http://dx.doi.org/10.1042/cs20060342.

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The intracellular signal transduction of AngII (angiotensin II) has been implicated in cardiovascular diseases, such as hypertension, atherosclerosis and restenosis after injury. AT1 receptor (AngII type-1 receptor), a G-protein-coupled receptor, mediates most of the physiological and pathophysiological actions of AngII, and this receptor is predominantly expressed in cardiovascular cells, such as VSMCs (vascular smooth muscle cells). AngII activates various signalling molecules, including G-protein-derived second messengers, protein kinases and small G-proteins (Ras, Rho, Rac etc), through th

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Passos-Silva, Danielle G., Thiago Verano-Braga, and Robson A. S. Santos. "Angiotensin-(1–7): beyond the cardio-renal actions." Clinical Science 124, no. 7 (2012): 443–56. http://dx.doi.org/10.1042/cs20120461.

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It is well known that the RAS (renin–angiotensin system) plays a key role in the modulation of many functions in the body. AngII (angiotensin II) acting on AT1R (type 1 AngII receptor) has a central role in mediating most of the actions of the RAS. However, over the past 10 years, several studies have presented evidence for the existence of a new arm of the RAS, namely the ACE (angiotensin-converting enzyme) 2/Ang-(1–7) [angiotensin-(1–7)]/Mas axis. Ang-(1–7) can be produced from AngI or AngII via endo- or carboxy-peptidases respectively. ACE2 appears to play a central role in Ang-(1–7) format

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Premilovac, Dino, Emily Attrill, Stephen Rattigan, Stephen M. Richards, Jeonga Kim, and Michelle A. Keske. "Acute, local infusion of angiotensin II impairs microvascular and metabolic insulin sensitivity in skeletal muscle." Cardiovascular Research 115, no. 3 (2018): 590–601. http://dx.doi.org/10.1093/cvr/cvy225.

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Abstract Aims Angiotensin II (AngII) is a potent vasoconstrictor implicated in both hypertension and insulin resistance. Insulin dilates the vasculature in skeletal muscle to increase microvascular blood flow and enhance glucose disposal. In the present study, we investigated whether acute AngII infusion interferes with insulin’s microvascular and metabolic actions in skeletal muscle. Methods and results Adult, male Sprague-Dawley rats received a systemic infusion of either saline, AngII, insulin (hyperinsulinaemic euglycaemic clamp), or insulin (hyperinsulinaemic euglycaemic clamp) plus AngII

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Kamal, Maud, Danielle Jacques, and Ghassan Bkaily. "Angiotensin II receptors’ modulation of calcium homeostasis in human vascular endothelial cells." Canadian Journal of Physiology and Pharmacology 95, no. 10 (2017): 1289–97. http://dx.doi.org/10.1139/cjpp-2017-0416.

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Angiotensin II (AngII) plays an important role in the regulation of vascular smooth muscle function. However, little is known about AngII and its receptors AT1 (AT1R) and AT2 (AT2R) and their modulation of intracellular calcium in vascular endothelial cells (VECs) in general and more particularly of human origin. Using western blots, our results showed that AT1Rs and AT2Rs are present in human VECs (hVECs). Using quantitative 3D confocal imaging, our results showed that AngII is present at the cytoplasmic and nucleoplasmic levels and its relative density is lower in the nucleoplasm. However, b

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Chandrashekar, Kiran, Arnaldo Lopez-Ruiz, Ramiro Juncos, et al. "The Modulatory Role of Heme Oxygenase on Subpressor Angiotensin II-Induced Hypertension and Renal Injury." International Journal of Hypertension 2012 (2012): 1–7. http://dx.doi.org/10.1155/2012/392890.

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Angiotensin II (AngII) causes hypertension (HTN) and promotes renal injury while simultaneously inducing reno-protective enzymes like heme oxygenase-1 (HO-1). We examined the modulatory role of HO on sub-pressor angiotensin II (SP-AngII) induced renal inflammation and injury. We first tested whether the SP-AngII-induced renal dysfunction, inflammation and injury are exacerbated by either preventing (chronic HO-1 inhibition) or reversing (late HO-1 inhibition) SP-AngII-induced HO (using tin protoporphyrin; SnPP). We next examined whether additional chronic or late induction of SP-AngII-induced

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Broekmans, Kathrin, Jan Giesen, Lukas Menges, Doris Koesling, and Michael Russwurm. "Angiotensin II-Induced Cardiovascular Fibrosis Is Attenuated by NO-Sensitive Guanylyl Cyclase1." Cells 9, no. 11 (2020): 2436. http://dx.doi.org/10.3390/cells9112436.

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In the NO/cGMP signaling cascade, relevant in the cardiovascular system, two NO-sensitive guanylyl cyclase (NO-GC) isoforms are responsible for NO-dependent cGMP generation. Here, the impact of the major NO-GC isoform, NO-GC1, on fibrosis development in the cardiovascular system was studied in NO-GC1-deficient mice treated with AngiotensinII (AngII), known to induce vascular and cardiac remodeling. Morphometric analysis of NO-GC1 KO’s aortae demonstrated an enhanced increase of perivascular area after AngII treatment accompanied by a higher aortic collagen1 mRNA content. Increased perivascular

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Chiu, Chiung-Zuan, Bao-Wei Wang, and Kou-Gi Shyu. "Angiotensin II and the JNK pathway mediate urotensin II expression in response to hypoxia in rat cardiomyocytes." Journal of Endocrinology 220, no. 3 (2014): 233–46. http://dx.doi.org/10.1530/joe-13-0261.

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Cardiomyocyte hypoxia causes cardiac hypertrophy through cardiac-restricted gene expression. Urotensin II (UII) cooperates with activating protein 1 (AP1) to regulate cardiomyocyte growth in response to myocardial injuries. Angiotensin II (AngII) stimulates UII expression, reactive oxygen species (ROS) production, and cardiac hypertrophy. This study aimed to evaluate the expression of UII, ROS, and AngII as well as their genetic transcription after hypoxia treatment in neonatal cardiomyocytes. Cultured neonatal rat cardiomyocytes were subjected to hypoxia for different time periods. UII (Uts2)

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Shechtman, Orit, Zhongjie Sun, Melvin J. Fregly, and Michael J. Katovich. "Increased tail artery vascular responsiveness to angiotensin II in cold-treated rats." Canadian Journal of Physiology and Pharmacology 77, no. 12 (1999): 974–79. http://dx.doi.org/10.1139/y99-107.

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Chronic exposure of rats to cold for 1-3 weeks results in a mild form of hypertension. The renin-angiotensin system (RAS) has been implicated in this model of cold-induced hypertension. Previously we have characterized the vascular responsiveness in cold-acclimated animals, using aortic tissue, and recent studies have focused on the thermoregulatory responses of angiotensin II (AngII), utilizing the tail artery of the rat. Therefore in the current study we evaluated the vascular responsiveness of cold-treated rats to AngII in both aorta and tail artery at 2 and 4 weeks of cold exposure (5 ± 2°

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da Silveira, Kátia D., Kênia S. Pompermayer Bosco, Lúcio R. L. Diniz, et al. "ACE2–angiotensin-(1–7)–Mas axis in renal ischaemia/reperfusion injury in rats." Clinical Science 119, no. 9 (2010): 385–94. http://dx.doi.org/10.1042/cs20090554.

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AngII (angiotensin II), ACE (angiotensin I-converting enzyme) and the AT1 receptor (AngII type 1 receptor) are associated with the inflammatory process and microvascular dysfunction of AKI (acute kidney injury) induced by renal I/R (ischaemia/reperfusion). However, Ang-(1–7) [angiotensin-(1–7)], ACE2 (angiotensin I-converting enzyme 2) and the Mas receptor also play a role in renal disease models. Therefore, in the present study, we have examined the renal profile of Ang-(1–7), ACE2 and the Mas receptor in renal I/R and compared them with that of AngII, ACE and the AT1 receptor. Male Wistar ra

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FRANCO, MARTHA, EDILIA TAPIA, JOSÉ SANTAMARÍA, et al. "Renal Cortical Vasoconstriction Contributes to Development of Salt-Sensitive Hypertension after Angiotensin II Exposure." Journal of the American Society of Nephrology 12, no. 11 (2001): 2263–71. http://dx.doi.org/10.1681/asn.v12112263.

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Abstract. Rats that are administered angiotensin II (AngII) for 2 wk develop persistent salt-sensitive hypertension, which can be prevented by the immunosuppressor mycophenolate mofetil (MMF) given during the AngII infusion. This study examined the contribution of glomerular hemodynamics (GFR dynamics) in the post-AngII hypertensive response to a high-salt diet (HSD) and the effect of MMF treatment. During AngII administration, rats developed severe hypertension (systolic BP [SBP], 185 ± 3.9 mmHg), proteinuria, afferent and efferent vasoconstriction, and glomerular hypertension. Rats that rece

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Ferreira, Rogério, Bernardo Gasperin, Joabel Santos, et al. "Angiotensin II profile and mRNA encoding RAS proteins during bovine follicular wave." Journal of the Renin-Angiotensin-Aldosterone System 12, no. 4 (2011): 475–82. http://dx.doi.org/10.1177/1470320311403786.

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Angiotensin II (AngII) has a role in ovarian follicle development, ovulation, and oocyte meiotic resumption. The objective of the present study was to characterise the AngII profile and the mRNA encoding RAS proteins in a bovine follicular wave. Cows were ovariectomised when the size between the largest (F1) and the second largest follicle (F2) was not statistically different (day 2), slightly different (day 3), or markedly different (day 4). AngII was measured in the follicular fluid and the mRNA abundance of genes encoding angiotensin-converting enzyme (ACE), (pro)renin receptor, and renin-b

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van der Kleij, Frank G. H., Paul E. de Jong, Rob H. Henning, Dick de Zeeuw, and Gerjan Navis. "Enhanced Responses of Blood Pressure, Renal Function, and Aldosterone to Angiotensin I in the DD Genotype Are Blunted by Low Sodium Intake." Journal of the American Society of Nephrology 13, no. 4 (2002): 1025–33. http://dx.doi.org/10.1681/asn.v1341025.

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ABSTRACT. Angiotensin-converting enzyme (ACE) activity is increased in the DD genotype, but the functional significance for renal function is unknown. Blunted responses of BP and proteinuria to ACE inhibition among DD renal patients during periods of high sodium intake were reported. It was therefore hypothesized that sodium status affects the phenotype in the ACE I/D polymorphism. The effects of angiotensin I (AngI) and AngII among 27 healthy subjects, with both low (50 mmol sodium/d) and liberal (200 mmol sodium/d) sodium intakes, were studied. Baseline mean arterial pressure (MAP) values, r

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Miyao, Masashi, Stephanie Cicalese, Tatsuo Kawai, et al. "Involvement of Senescence and Mitochondrial Fission in Endothelial Cell Pro-Inflammatory Phenotype Induced by Angiotensin II." International Journal of Molecular Sciences 21, no. 9 (2020): 3112. http://dx.doi.org/10.3390/ijms21093112.

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Angiotensin II (AngII) has a crucial role in cardiovascular pathologies, including endothelial inflammation and premature vascular aging. However, the precise molecular mechanism underlying aging-related endothelial inflammation induced by AngII remains elusive. Here, we have tested a hypothesis in cultured rat aortic endothelial cells (ECs) that the removal of AngII-induced senescent cells, preservation of proteostasis, or inhibition of mitochondrial fission attenuates the pro-inflammatory EC phenotype. AngII stimulation in ECs resulted in cellular senescence assessed by senescence-associated

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Saha, Sarama, Stefan Bornstein, Juergen Graessler, Sasanka Chakrabarti, and Steffi Kopprasch. "Aldosterone Hypothesis for Cognitive Impairment in Diabetes Mellitus." Hormone and Metabolic Research 49, no. 09 (2017): 716–18. http://dx.doi.org/10.1055/s-0043-115226.

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AbstractIncreased plasma aldosterone concentration is significantly associated with dementia, which is accentuated by diabetes mellitus (DM). Angiotensin II (AngII) deteriorates cognitive function through neuronal degradation. Lipoproteins, a major source of cholesterol for aldosterone biosynthesis, undergo glycoxidative modifications in the presence of hyperglycemia. We hypothesize that there would be a pathophysiological link between diabetically-modified lipoproteins, angiotensin II, and increased plasma aldosterone concentration for induction of cognitive impairment. Glycoxidized lipoprote

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Zhao, Yunfeng, Kun Liu, Delu Yin, and Zhaoheng Lin. "Angiopoietin-Like 7 Contributes to Angiotensin II-Induced Proliferation, Inflammation and Apoptosis in Vascular Smooth Muscle Cells." Pharmacology 104, no. 5-6 (2019): 226–34. http://dx.doi.org/10.1159/000501296.

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Introduction: Angiotensin II (AngII) induces hypertension and pathophysiological vascular thickening and atherosclerosis. This study aims to validate the effects of Angiopoietin-like 7 (ANGPTL7) in AngII-induced hypertension. Methods: ANGPTL7 in blood samples were determined by quantitative real-time polymerase chain reaction. AngII-induced cell growth were detected by CCK-8. Cell cycle arrest and cell apoptosis by downregulation of ANGPTL7 were detected by flow cytometric assay. AngII-induced inflammation was evaluated by Western blotting and ELISA. Results: ANGPTL7 was highly expressed in pa

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Hao, QingQing, Xu Chen, XiaoYu Wang, Bo Dong, and ChuanHua Yang. "Curcumin Attenuates Angiotensin II-Induced Abdominal Aortic Aneurysm by Inhibition of Inflammatory Response and ERK Signaling Pathways." Evidence-Based Complementary and Alternative Medicine 2014 (2014): 1–10. http://dx.doi.org/10.1155/2014/270930.

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Background and Objectives. Curcumin has long been used to treat age-related diseases, such as atherosclerosis and coronary heart disease. In this study, we explored the effects of curcumin on the development of abdominal aortic aneurysm (AAA).Methods. ApoE−/−mice were randomly divided into 3 groups: AngII group, AngII + curcumin (AngII + Cur) group (100 mg/kg/d), and the control group. Miniosmotic pumps were implanted subcutaneously in ApoE−/−mice to deliver AngII for 28 days. After 4-week treatment, abdominal aortas with AAA were obtained for H&E staining, immunohistochemistry, and Wester

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Ferrario, Carlos Maria, Sarfaraz Ahmad, Sayaka Nagata, et al. "An evolving story of angiotensin-II-forming pathways in rodents and humans." Clinical Science 126, no. 7 (2013): 461–69. http://dx.doi.org/10.1042/cs20130400.

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Lessons learned from the characterization of the biological roles of Ang-(1–7) [angiotensin-(1–7)] in opposing the vasoconstrictor, proliferative and prothrombotic actions of AngII (angiotensin II) created an underpinning for a more comprehensive exploration of the multiple pathways by which the RAS (renin–angiotensin system) of blood and tissues regulates homoeostasis and its altered state in disease processes. The present review summarizes the progress that has been made in the novel exploration of intermediate shorter forms of angiotensinogen through the characterization of the expression a

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Kramer, RE, TV Robinson, EG Schneider, and TG Smith. "Direct modulation of basal and angiotensin II-stimulated aldosterone secretion by hydrogen ions." Journal of Endocrinology 166, no. 1 (2000): 183–94. http://dx.doi.org/10.1677/joe.0.1660183.

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Disturbances in acid-base balance in vivo are associated with changes in plasma aldosterone concentration, and in vitro changes in extracellular pH (pH(o)) influence the secretion of aldosterone by adrenocortical tissue or glomerulosa cells. There is considerable disparity, however, as to the direction of the effect. Furthermore, the mechanisms by which pH(o) independently affects aldosterone secretion or interacts with other secretagogues are not defined. Thus, bovine glomerulosa cells maintained in primary monolayer culture were used to examine the direct effects of pH(o) on cytosolic free c

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Rao, G. N., B. Lassègue, R. W. Alexander, and K. K. Griendling. "Angiotensin II stimulates phosphorylation of high-molecular-mass cytosolic phospholipase A2 in vascular smooth-muscle cells." Biochemical Journal 299, no. 1 (1994): 197–201. http://dx.doi.org/10.1042/bj2990197.

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Phospholipase A2 (PLA2) may be one of the major components involved in cell signalling and proliferation, as suggested by recent studies. In this paper we show that the potent vasoconstrictor and hypertrophic agent angiotensin II (AngII) activates cytosolic PLA2 (cPLA2) in vascular smooth-muscle cells. AngII induced a rapid time-dependent release of [3H]arachidonic acid from prelabelled cells that was inhibited by mepacrine, a PLA2 inhibitor. AngII treatment of intact cells also activated a cPLA2, as measured in cell-free extracts by the release of radiolabelled arachidonic acid from exogenous

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