Angiotensinogen: An alpha-globulin of about 453 amino acids, depending on the species. It is produced by the liver and secreted into blood circulation. Angiotensinogen is the inactive precursor of natural angiotensins. Upon successive enzyme cleavages, angiotensinogen yields angiotensin I, II, and III with amino acids numbered at 10, 8, and 7, respectively.Angiotensins: Oligopeptides which are important in the regulation of blood pressure (VASOCONSTRICTION) and fluid homeostasis via the RENIN-ANGIOTENSIN SYSTEM. These include angiotensins derived naturally from precursor ANGIOTENSINOGEN, and those synthesized.Renin-Angiotensin System: A BLOOD PRESSURE regulating system of interacting components that include RENIN; ANGIOTENSINOGEN; ANGIOTENSIN CONVERTING ENZYME; ANGIOTENSIN I; ANGIOTENSIN II; and angiotensinase. Renin, an enzyme produced in the kidney, acts on angiotensinogen, an alpha-2 globulin produced by the liver, forming ANGIOTENSIN I. Angiotensin-converting enzyme, contained in the lung, acts on angiotensin I in the plasma converting it to ANGIOTENSIN II, an extremely powerful vasoconstrictor. Angiotensin II causes contraction of the arteriolar and renal VASCULAR SMOOTH MUSCLE, leading to retention of salt and water in the KIDNEY and increased arterial blood pressure. In addition, angiotensin II stimulates the release of ALDOSTERONE from the ADRENAL CORTEX, which in turn also increases salt and water retention in the kidney. Angiotensin-converting enzyme also breaks down BRADYKININ, a powerful vasodilator and component of the KALLIKREIN-KININ SYSTEM.Renin: A highly specific (Leu-Leu) endopeptidase that generates ANGIOTENSIN I from its precursor ANGIOTENSINOGEN, leading to a cascade of reactions which elevate BLOOD PRESSURE and increase sodium retention by the kidney in the RENIN-ANGIOTENSIN SYSTEM. The enzyme was formerly listed as EC 3.4.99.19.Angiotensin II: An octapeptide that is a potent but labile vasoconstrictor. It is produced from angiotensin I after the removal of two amino acids at the C-terminal by ANGIOTENSIN CONVERTING ENZYME. The amino acid in position 5 varies in different species. To block VASOCONSTRICTION and HYPERTENSION effect of angiotensin II, patients are often treated with ACE INHIBITORS or with ANGIOTENSIN II TYPE 1 RECEPTOR BLOCKERS.Peptidyl-Dipeptidase A: A peptidyl-dipeptidase that catalyzes the release of a C-terminal dipeptide, -Xaa-*-Xbb-Xcc, when neither Xaa nor Xbb is Pro. It is a Cl(-)-dependent, zinc glycoprotein that is generally membrane-bound and active at neutral pH. It may also have endopeptidase activity on some substrates. (From Enzyme Nomenclature, 1992) EC 3.4.15.1.Hypertension: Persistently high systemic arterial BLOOD PRESSURE. Based on multiple readings (BLOOD PRESSURE DETERMINATION), hypertension is currently defined as when SYSTOLIC PRESSURE is consistently greater than 140 mm Hg or when DIASTOLIC PRESSURE is consistently 90 mm Hg or more.Angiotensin I: A decapeptide that is cleaved from precursor angiotensinogen by RENIN. Angiotensin I has limited biological activity. It is converted to angiotensin II, a potent vasoconstrictor, after the removal of two amino acids at the C-terminal by ANGIOTENSIN CONVERTING ENZYME.Receptor, Angiotensin, Type 1: An angiotensin receptor subtype that is expressed at high levels in a variety of adult tissues including the CARDIOVASCULAR SYSTEM, the KIDNEY, the ENDOCRINE SYSTEM and the NERVOUS SYSTEM. Activation of the type 1 angiotensin receptor causes VASOCONSTRICTION and sodium retention.Blood Pressure: PRESSURE of the BLOOD on the ARTERIES and other BLOOD VESSELS.Mestranol: The 3-methyl ether of ETHINYL ESTRADIOL. It must be demethylated to be biologically active. It is used as the estrogen component of many combination ORAL CONTRACEPTIVES.RNA, Messenger: RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.Receptors, Angiotensin: Cell surface proteins that bind ANGIOTENSINS and trigger intracellular changes influencing the behavior of cells.Kidney: Body organ that filters blood for the secretion of URINE and that regulates ion concentrations.Polymorphism, Genetic: The regular and simultaneous occurrence in a single interbreeding population of two or more discontinuous genotypes. The concept includes differences in genotypes ranging in size from a single nucleotide site (POLYMORPHISM, SINGLE NUCLEOTIDE) to large nucleotide sequences visible at a chromosomal level.Methyltestosterone: A synthetic hormone used for androgen replacement therapy and as an hormonal antineoplastic agent (ANTINEOPLASTIC AGENTS, HORMONAL).Receptor, Angiotensin, Type 2: An angiotensin receptor subtype that is expressed at high levels in fetal tissues. Many effects of the angiotensin type 2 receptor such as VASODILATION and sodium loss are the opposite of that of the ANGIOTENSIN TYPE 1 RECEPTOR.Animals, Genetically Modified: ANIMALS whose GENOME has been altered by GENETIC ENGINEERING, or their offspring.Genotype: The genetic constitution of the individual, comprising the ALLELES present at each GENETIC LOCUS.Losartan: An antagonist of ANGIOTENSIN TYPE 1 RECEPTOR with antihypertensive activity due to the reduced pressor effect of ANGIOTENSIN II.Rats, Inbred WKY: A strain of Rattus norvegicus used as a normotensive control for the spontaneous hypertensive rats (SHR).Rats, Inbred SHR: A strain of Rattus norvegicus with elevated blood pressure used as a model for studying hypertension and stroke.Rats, Transgenic: Laboratory rats that have been produced from a genetically manipulated rat EGG or rat EMBRYO, MAMMALIAN. They contain genes from another species.Kidney Tubules, Proximal: The renal tubule portion that extends from the BOWMAN CAPSULE in the KIDNEY CORTEX into the KIDNEY MEDULLA. The proximal tubule consists of a convoluted proximal segment in the cortex, and a distal straight segment descending into the medulla where it forms the U-shaped LOOP OF HENLE.Rats, Sprague-Dawley: A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.Eosinophil Major Basic Protein: One of several basic proteins released from EOSINOPHIL cytoplasmic granules. Eosinophil major basic protein is a 14-kDa cytotoxic peptide with a pI of 10.9. In addition to its direct cytotoxic effects, it stimulates the release of variety of INFLAMMATION MEDIATORS.Subfornical Organ: A structure, situated close to the intraventricular foramen, which induces DRINKING BEHAVIOR after stimulation with ANGIOTENSIN II.Alleles: Variant forms of the same gene, occupying the same locus on homologous CHROMOSOMES, and governing the variants in production of the same gene product.Angiotensin II Type 1 Receptor Blockers: Agents that antagonize ANGIOTENSIN II TYPE 1 RECEPTOR. Included are ANGIOTENSIN II analogs such as SARALASIN and biphenylimidazoles such as LOSARTAN. Some are used as ANTIHYPERTENSIVE AGENTS.Sodium Chloride, Dietary: Sodium chloride used in foods.Captopril: A potent and specific inhibitor of PEPTIDYL-DIPEPTIDASE A. It blocks the conversion of ANGIOTENSIN I to ANGIOTENSIN II, a vasoconstrictor and important regulator of arterial blood pressure. Captopril acts to suppress the RENIN-ANGIOTENSIN SYSTEM and inhibits pressure responses to exogenous angiotensin.Gene Expression Regulation: Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control (induction or repression) of gene action at the level of transcription or translation.TetrazolesNephrectomy: Excision of kidney.Glomerulonephritis, IGA: A chronic form of glomerulonephritis characterized by deposits of predominantly IMMUNOGLOBULIN A in the mesangial area (GLOMERULAR MESANGIUM). Deposits of COMPLEMENT C3 and IMMUNOGLOBULIN G are also often found. Clinical features may progress from asymptomatic HEMATURIA to END-STAGE KIDNEY DISEASE.Gene Frequency: The proportion of one particular in the total of all ALLELES for one genetic locus in a breeding POPULATION.Antibodies: Immunoglobulin molecules having a specific amino acid sequence by virtue of which they interact only with the ANTIGEN (or a very similar shape) that induced their synthesis in cells of the lymphoid series (especially PLASMA CELLS).Antibody Specificity: The property of antibodies which enables them to react with some ANTIGENIC DETERMINANTS and not with others. Specificity is dependent on chemical composition, physical forces, and molecular structure at the binding site.Molecular Sequence Data: Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.Recombinant Proteins: Proteins prepared by recombinant DNA technology.Myocardium: The muscle tissue of the HEART. It is composed of striated, involuntary muscle cells (MYOCYTES, CARDIAC) connected to form the contractile pump to generate blood flow.Heart Ventricles: The lower right and left chambers of the heart. The right ventricle pumps venous BLOOD into the LUNGS and the left ventricle pumps oxygenated blood into the systemic arterial circulation.Heart Failure: A heterogeneous condition in which the heart is unable to pump out sufficient blood to meet the metabolic need of the body. Heart failure can be caused by structural defects, functional abnormalities (VENTRICULAR DYSFUNCTION), or a sudden overload beyond its capacity. Chronic heart failure is more common than acute heart failure which results from sudden insult to cardiac function, such as MYOCARDIAL INFARCTION.Angiotensin-Converting Enzyme Inhibitors: A class of drugs whose main indications are the treatment of hypertension and heart failure. They exert their hemodynamic effect mainly by inhibiting the renin-angiotensin system. They also modulate sympathetic nervous system activity and increase prostaglandin synthesis. They cause mainly vasodilation and mild natriuresis without affecting heart rate and contractility.Albuminuria: The presence of albumin in the urine, an indicator of KIDNEY DISEASES.Aryldialkylphosphatase: An enzyme which catalyzes the hydrolysis of an aryl-dialkyl phosphate to form dialkyl phosphate and an aryl alcohol. It can hydrolyze a broad spectrum of organophosphate substrates and a number of aromatic carboxylic acid esters. It may also mediate an enzymatic protection of LOW DENSITY LIPOPROTEINS against oxidative modification and the consequent series of events leading to ATHEROMA formation. The enzyme was previously regarded to be identical with Arylesterase (EC 3.1.1.2).Diabetic Nephropathies: KIDNEY injuries associated with diabetes mellitus and affecting KIDNEY GLOMERULUS; ARTERIOLES; KIDNEY TUBULES; and the interstitium. Clinical signs include persistent PROTEINURIA, from microalbuminuria progressing to ALBUMINURIA of greater than 300 mg/24 h, leading to reduced GLOMERULAR FILTRATION RATE and END-STAGE RENAL DISEASE.Diabetes Mellitus, Type 2: A subclass of DIABETES MELLITUS that is not INSULIN-responsive or dependent (NIDDM). It is characterized initially by INSULIN RESISTANCE and HYPERINSULINEMIA; and eventually by GLUCOSE INTOLERANCE; HYPERGLYCEMIA; and overt diabetes. Type II diabetes mellitus is no longer considered a disease exclusively found in adults. Patients seldom develop KETOSIS but often exhibit OBESITY.Research Support, U.S. Gov't, Non-P.H.S.Research Support, U.S. Gov't, P.H.S.Research Support, Non-U.S. Gov'tResearch Support, U.S. GovernmentKidney Tubules, Collecting: Straight tubes commencing in the radiate part of the kidney cortex where they receive the curved ends of the distal convoluted tubules. In the medulla the collecting tubules of each pyramid converge to join a central tube (duct of Bellini) which opens on the summit of the papilla.Research Support, American Recovery and Reinvestment Act

Angiotensinogen gene polymorphisms M235T/T174M: no excess transmission to hypertensive Chinese. (1/836)

The gene encoding angiotensinogen (AGT) has been widely studied as a candidate gene for hypertension. Most studies to date have relied on case-control analysis to test for an excess of AGT variants among hypertensive cases compared with normotensive controls. However, with this design, nothing guarantees that a positive finding is due to actual allelic association as opposed to an inappropriate control population. To avoid this difficulty in our study of essential hypertension in Anqing, China, we tested AGT variants using the transmission/disequilibrium test, a procedure that bypasses the need for a control sample by testing for excessive transmission of a genetic variant from parents heterozygous for that variant. We analyzed two AGT polymorphisms, M235T and T174M, which have been associated with essential hypertension in whites and Japanese, using data on 335 hypertensive subjects from 315 nuclear families and their parents. Except in the group of subjects younger than 25 years, M235 and T174 were the more frequently transmitted alleles. We found that 194 parents heterozygous for M235T transmitted M235 106 times (P=0.22) and that 102 parents heterozygous for T174M transmitted T174 60 times (P=0.09). Stratifying offspring by gender, M235 and T174 were transmitted 60 of 106 times (P=0.21) and 44 of 75 times (P=0.17), respectively, in men, and 46 of 88 times (P=0.75) and 16 of 27 times (P=0.44), respectively, in women. Our results were also negative in all age groups and for the affected offspring with blood pressure values >/=160/95 mm Hg. Thus, this study provides no evidence that either allele of M235T or T174M contributes to hypertension in this Chinese population.  (+info)

Insulin-like growth factor-1 induces Mdm2 and down-regulates p53, attenuating the myocyte renin-angiotensin system and stretch-mediated apoptosis. (2/836)

Insulin-like growth factor (IGF)-1 inhibits apoptosis, but its mechanism is unknown. Myocyte stretching activates p53 and p53-dependent genes, leading to the formation of angiotensin II (Ang II) and apoptosis. Therefore, this in vitro system was used to determine whether IGF-1 interfered with p53 function and the local renin-angiotensin system (RAS), decreasing stretch-induced cell death. A single dose of 200 ng/ml IGF-1 at the time of stretching decreased myocyte apoptosis 43% and 61% at 6 and 20 hours. Ang II concentration was reduced 52% at 20 hours. Additionally, p53 DNA binding to angiotensinogen (Aogen), AT1 receptor, and Bax was markedly down-regulated by IGF-1 via the induction of Mdm2 and the formation of Mdm2-p53 complexes. Concurrently, the quantity of p53, Aogen, renin, AT1 receptor, and Bax was reduced in stretched myocytes exposed to IGF-1. Conversely, Bcl-2 and the Bcl-2-to-Bax protein ratio increased. The effects of IGF-1 on cell death, Ang II synthesis, and Bax protein were the consequence of Mdm2-induced down-regulation of p53 function. In conclusion, the anti-apoptotic impact of IGF-1 on stretched myocytes was mediated by its capacity to depress p53 transcriptional activity, which limited Ang II formation and attenuated the susceptibility of myocytes to trigger their endogenous cell death pathway.  (+info)

Blood pressure reduction and diabetes insipidus in transgenic rats deficient in brain angiotensinogen. (3/836)

Angiotensin produced systemically or locally in tissues such as the brain plays an important role in the regulation of blood pressure and in the development of hypertension. We have established transgenic rats [TGR(ASrAOGEN)] expressing an antisense RNA against angiotensinogen mRNA specifically in the brain. In these animals, the brain angiotensinogen level is reduced by more than 90% and the drinking response to intracerebroventricular renin infusions is decreased markedly compared with control rats. Blood pressure of transgenic rats is lowered by 8 mmHg (1 mmHg = 133 Pa) compared with control rats. Crossbreeding of TGR(ASrAOGEN) with a hypertensive transgenic rat strain exhibiting elevated angiotensin II levels in tissues results in a marked attenuation of the hypertensive phenotype. Moreover, TGR(ASrAOGEN) exhibit a diabetes insipidus-like syndrome producing an increased amount of urine with decreased osmolarity. The observed reduction in plasma vasopressin by 35% may mediate these phenotypes of TGR(ASrAOGEN). This new animal model presenting long-term and tissue-specific down-regulation of angiotensinogen corroborates the functional significance of local angiotensin production in the brain for the central regulation of blood pressure and for the pathogenesis of hypertension.  (+info)

Local renin-angiotensin system is involved in K+-induced aldosterone secretion from human adrenocortical NCI-H295 cells. (4/836)

NCI-H295, a human adrenocarcinoma cell line, has been proposed as a model system to define the role of the renin-angiotensin system in the regulation of aldosterone production in humans. Because the precise cellular localization of the components of the renin-angiotensin system in human adrenal cortical cells remains unclear, we investigated their localization in this defined cell system. NCI-H295 cells expressed both angiotensinogen and renin as shown by reverse transcriptase polymerase chain reaction and immunohistochemistry. Human angiotensin-converting enzyme (ACE) was not detectable by immunocytochemistry, ACE binding, or reverse transcriptase polymerase chain reaction. However, 3.5 mmol/L K+ stimulated the formation of both angiotensin I and angiotensin II 1. 9- and 2.5-fold, respectively, and increased aldosterone release 3. 0-fold. The K+-induced stimulation of aldosterone release was decreased by captopril and enalaprilat (24% and 26%, respectively) and by the angiotensin type 1 (AT1)-receptor antagonist losartan (28%). Angiotensin II-induced stimulation of aldosterone release was abolished by losartan treatment. Specific [125I]Sar1-angiotensin II binding was detected by receptor autoradiography. The binding of [125I]Sar1-angiotensin II was completely displaced by the AT1 antagonist losartan but not by the AT2 receptor ligand PD 123319, confirming the expression of angiotensin II AT1 receptors in NCI-H295 cells. Our results demonstrate that NCI-H295 cells express most of the components of the renin-angiotensin system. Our failure to detect ACE, however, suggests that the production of angiotensin II in NCI-H295 cells may be ACE independent. NCI-H295 cells are able to produce angiotensin II, and K+ increases aldosterone secretion in part through an angiotensin-mediated pathway. The production of angiotensin II in NCI-H295 cells demonstrates that this human cell line can be useful to characterize the role of locally produced angiotensin II in the regulation of aldosterone release.  (+info)

The renal lesions that develop in neonatal mice during angiotensin inhibition mimic obstructive nephropathy. (5/836)

BACKGROUND: Inhibition of angiotensin action, pharmacologically or genetically, during the neonatal period leads to renal anomalies involving hypoplastic papilla and dilated calyx. Recently, we documented that angiotensinogen (Agt -/-) or angiotensin type 1 receptor nullizygotes (Agtr1 -/-) do not develop renal pelvis nor ureteral peristaltic movement, both of which are essential for isolating the kidney from the high downstream ureteral pressure. We therefore examined whether these renal anomalies could be characterized as "obstructive" nephropathy. METHODS: Agtr1 -/- neonatal mice were compared with wild-type neonates, the latter subjected to surgical complete unilateral ureteral ligation (UUO), by analyzing morphometrical, immunohistochemical, and molecular indices. Agtr1 -/- mice were also subjected to a complete UUO and were compared with wild-type UUO mice by quantitative analysis. To assess the function of the urinary tract, baseline pelvic and ureteral pressures were measured. RESULTS: The structural anomalies were qualitatively indistinguishable between the Agtr1 -/- without surgical obstruction versus the wild type with complete UUO. Thus, in both kidneys, the calyx was enlarged, whereas the papilla was atrophic; tubulointerstitial cells underwent proliferation and also apoptosis. Both were also characterized by interstitial macrophage infiltration and fibrosis, and within the local lesion, transforming growth factor-beta 1, platelet-derived growth factor-A and insulin-like growth factor-1 were up-regulated, whereas epidermal growth factor was down-regulated. Moreover, quantitative differences that exist between mutant kidneys without surgical obstruction and wild-type kidneys with surgical UUO were abolished when both underwent the same complete surgical UUO. The hydraulic baseline pressure was always lower in the pelvis than that in the ureter in the wild type, whereas this pressure gradient was reversed in the mutant. CONCLUSION: The abnormal kidney structure that develops in neonates during angiotensin inhibition is attributed largely to "functional obstruction" of the urinary tract caused by the defective development of peristaltic machinery.  (+info)

Molecular mechanism(s) of action of isoproterenol on the expression of the angiotensinogen gene in opossum kidney proximal tubular cells. (6/836)

BACKGROUND: beta-adrenoceptors are present in the renal proximal tubules. We have previously reported that isoproterenol stimulates the accumulation of intracellular cAMP and the expression of the angiotensinogen (ANG) gene in opossum kidney (OK) proximal tubular cells via the beta 1-adrenoceptor. We hypothesized that the molecular mechanism(s) of action of isoproterenol on the expression of the ANG gene is mediated via the interaction of the phosphorylated cAMP-responsive element binding protein (CREB) and the cAMP-responsive element (CRE; that is, ANG N-806/-779) in the 5'-flanking region of the rat ANG gene. METHODS: The fusion genes containing the putative ANG-CRE of the rat ANG gene inserted upstream of the rat ANG basal promoter (ANG N-53/+18) fused to a human growth hormone (hGH) gene as reporter were stably cotransfected, with or without the plasmid containing the cDNA for 43 kDa CREB, into the OK cells. The effect of various agonists and antagonists of adrenoceptors on the expression of the fusion genes was evaluated by the amount of immunoreactive hGH secreted into the culture medium. The interactions of OK cellular nuclear protein(s) with the ANG N-806/779 were determined by gel mobility shift assays and by Southwestern and Western blot analysis. RESULTS: The addition of isoproterenol, forskolin, or 8-Bromo-cAMP (8-Br-cAMP) stimulated the expression of pOGH (ANG N-806/-779/-53/+18) by 135, 150, and 160%, respectively, but not mutants of the ANG N-806/-779. The stimulatory effect of isoproterenol was blocked in the presence of propranolol, Rp-cAMP, and atenolol, but not by the presence of stauro-sporine, U73122, and ICI 118,551. Transient transfection of the plasmid containing the cDNA for the catalytic subunit of protein kinase A further enhanced the stimulatory effect of 43 kDa CREB on the expression of the fusion gene. The gel mobility shift assays revealed the the nuclear protein(s) of OK cells binds to the radioactive-labeled ANG N-806/-779. The binding of the labeled ANG N-806/-779 to the OK cell nuclear protein(s) was displaced by unlabeled ANG N-806/-779, but not by the CRE of the somatostatin gene, the CRE of the tyrosine amino-transferase gene, or the mutants of the ANG N-806/-779. Southwestern blot analysis revealed that the labeled ANG N-806/-779 binds to two nuclear species of 43 and 35 kDa proteins. Western blot analysis, however, revealed that rabbit polyclonal antibodies against the 43 kDa CREB interacted with only the 43 kDa molecular species but not with the 35 kDa species. CONCLUSION: These studies demonstrate that the stimulatory effect of isoproterenol on the expression of the ANG gene may be mediated, at least in part, via the interaction of the phosphorylated CREB and the CRE in the 5'-flanking region of the rat ANG gene. The novel 35 kDa nuclear protein that is immunologically different from the 43 kDa CREB may also play a role in the expression of the ANG gene.  (+info)

Homeostasis in mice with genetically decreased angiotensinogen is primarily by an increased number of renin-producing cells. (7/836)

Here we investigate the biochemical, molecular, and cellular changes directed toward blood pressure homeostasis that occur in the endocrine branch of the renin-angiotensin system of mice having one angiotensinogen gene inactivated. No compensatory up-regulation of the remaining normal allele occurs in the liver, the main tissue of angiotensinogen synthesis. No significant changes occur in expression of the genes coding for the angiotensin converting enzyme or the major pressor-mediating receptor for angiotensin, but plasma renin concentration in the mice having only one copy of the angiotensinogen gene is greater than twice wild-type. This increase is mediated primarily by a modest increase in the proportion of renal glomeruli producing renin in their juxtaglomerular apparatus and by four times wild-type numbers of renin-producing cells along afferent arterioles of the glomeruli rather than by up-regulating renin production in cells already committed to its synthesis.  (+info)

In vivo enzymatic assay reveals catalytic activity of the human renin precursor in tissues. (8/836)

The aspartyl protease renin is secreted into the circulation of mammals in 2 forms: the proteolytically processed active form of the enzyme and the precursor form, prorenin. Prorenin has no detectable enzymatic activity in the circulation, but it is the exclusive form of the enzyme produced by several tissues that also produce the other components of the renin enzymatic cascade (renin-angiotensin system). To test whether prorenin might be enzymatically active in these tissues, transgenic mice expressing the human renin substrate (angiotensinogen) exclusively in the pituitary gland were mated to mice expressing either active human renin or prorenin in the same tissue. Measurement of in vivo product formation in pituitary glands of double-transgenic mice revealed that human prorenin was enzymatically active, and Western blot analysis demonstrated that this prorenin was in the precursor form with its prosegment attached. This in vivo enzymatic assay demonstrates for the first time that human prorenin can be activated within tissues by nonproteolytic means, where it could contribute to the activity of a localized renin-angiotensin system.  (+info)

The presence of angiotensinogen messenger RNA (mRNA) was assessed in total RNA extracted from hepatoma, glioma, neuroblastoma, and glioma-neuroblastoma hybrid cell lines. Total RNA from 1 X 10(7) cells was extracted, transferred to a membrane, and hybridized with a 32P-labeled, full-length (1650-base pair) rat angiotensinogen complementary DNA (cDNA). Angiotensinogen RNA sequences could be definitively detected only in hepatoma cells. Steroids were used in an attempt to increase the angiotensinogen mRNA level. Dexamethasone (2 X 10(-6) M) or 17 beta-estradiol (1 X 10(-7) M) was added to the cultures 18 to 24 hours prior to harvest. Dexamethasone treatment of the hepatoma cells resulted in a large increase in angiotensinogen mRNA, whereas estradiol had no effect. Steroids failed to induce detectable levels of angiotensinogen mRNA in total RNA from the other cell lines. That the RNA was intact was ensured by hybridizing duplicate Northern blots to a 32P-labeled actin cDNA. Actin mRNA sequences ...
TY - JOUR. T1 - Glucocorticoid and thyroid hormone regulation of angiotensinogen gene expression in a pancreatic islet cell line.. AU - Brasier, A. R.. AU - Philippe, J.. AU - Campbell, D. J.. AU - Habener, J. F.. PY - 1986/12/1. Y1 - 1986/12/1. N2 - The renin-angiotensin system is an important regulator of blood pressure and volume homeostasis in mammals. Angiotensinogen, a precursor of the octapeptide angiotensin II and an effector of the renin-angiotensin system, is synthesized in numerous rat tissues. Angiotensinogen is expressed in an islet cell line (RIN 1056A) derived from a rat pancreatic tumor. Angiotensinogen mRNA detected by Northern analysis is abundant in the cell line and is approximately 200 bases longer than the mRNA isolated from rat liver, due to both a longer poly(A) tract and the use of a second polyadenylation site. Dexamethasone is a potent inducer of angiotensinogen mRNA, producing a progressive accumulation from 3 to 96 hr in culture (9-fold above control levels). The ...
Angiotensinogen messenger RNA (mRNA) levels were measured in the brain (hypothalamus, lower brain stem, cerebellum), liver, kidneys, and adrenal glands of rats made hypertensive by ligation of the aorta between the renal arteries. We also measured renin mRNA in the kidneys of these renal hypertensive rats. The early phase of hypertension (day 6) was associated with significant increases in plasma renin activity and levels of circulating angiotensin II. The circulating renin-angiotensin system was not activated in the later phase of hypertension (day 24). Angiotensinogen mRNA levels were elevated in the lower brain stem of hypertensive rats at both stages of hypertension. In contrast, angiotensinogen mRNA levels in the hypothalamus were increased only at day 6 after aortic ligation. Decreased levels of angiotensinogen mRNA were observed in the cerebellum in both the early and later phases of the hypertension. Angiotensinogen mRNA levels in the adrenal gland below the ligature fell in the early ...
TY - JOUR. T1 - Hyperglycemia modulates angiotensinogen gene expression. AU - Gabriely, Ilan. AU - Yang, Xiao Man. AU - Cases, Jane A.. AU - Ma, Xiao Hui. AU - Rossetti, Luciano. AU - Barzilai, Nir. PY - 2001/10/2. Y1 - 2001/10/2. N2 - Elevated plasma angiotensinogen (AGT) levels have been demonstrated in insulin-resistant states such as obesity and type 2 diabetes mellitus (DM2), conditions that are directly correlated to hypertension. We examined whether hyperinsulinemia or hyperglycemia may modulate fat and liver AGT gene expression and whether obesity and insulin resistance are associated with abnormal AGT regulation. In addition, because the hexosamine biosynthetic pathway is considered to function as a biochemical sensor of intracellular nutrient availability, we hypothesized that activation of this pathway would acutely mediate in vivo the induction of AGT gene expression in fat and liver. We studied chronically catheterized lean (∼300 g) and obese (∼450 g) Sprague-Dawley rats in four ...
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 ...
Buy our Recombinant Human Angiotensinogen protein. Ab191974 is a full length protein produced in HEK 293 cells and has been validated in SDS-PAGE, HPLC. Abcam…
Acetyl Angiotensinogen (1-14),porcine, The protein encoded by the Angiotensinogen gene is known as pre-angiotensinogen or angiotensinogen precursor.
The studies in this thesis describe the development of a microarray based minisequencing system and its application to highly parallel genotyping of single nucleotide polymorphisms. The technical developments included identification of a three-dimensional microarray surface coating with high binding capacity for oligonucleotides modified with amino groups as the most optimal one for the system. The system was also established for multiplexed, reproducible quantitative analysis of SNP alleles both on the level of DNA and RNA. The sensitivity of the system to distinguish SNP alleles present as a minority in a mixed sample was found to be 1-6%.. The microarray based minisequencing system was applied in a pharmacogenetic study on antihypertensive drug response. A panel of 74 SNPs located in candidate genes related to blood pressure regulation were genotyped in DNA samples from hypertensive patients that had been treated with the antihypertensive drugs irbesartan or atenolol. Multiple regression ...
Human angiotensinogen has been purified 390-fold from serum by a rapid high-yielding procedure that involved chromatography on Blue Sepharose, phenyl-Sepharose, hydroxyapatite and immobilized 5-hydroxytryptamine (5-HT). Angiotensinogen was specifically bound to immobilized 5-HT, which effected a partial resolution into multiple forms, which were also evident when analysed by SDS/polyacrylamide-gel electrophoresis (Mr 59,400, 60,600, 62,600 and 63,800). This heterogeneity was confirmed by resolution into six main bands on isoelectric focusing, ranging from pI 4.40 to 4.82. N-terminal analysis, digestion with human renal renin and deglycosylation studies implied that the preparation comprised several forms of angiotensinogen, varying in their degree of glycosylation. The presence of sialic acid was shown to be a major factor in determining the heterogeneity. ...
|p|Acetyl Angiotensinogen (1-14),porcine, (C87H125N21O21) is a peptide with the sequence AC-ASP-ARG-VAL-TYR-ILE-HIS-PRO-PHE-HIS-LEU-LEU-VAL-TYR-SER-OH, MW= 1801.05. The protein encoded by the Angiotensinogen gene is known as pre-angiotensinogen or angiote
BACKGROUND: The relationship between circulating levels of angiotensinogen and hypertension in the epidemiologic setting has not been studied much. Recent findings related to the association between hypertension and polymorphisms of the angiotensinogen gene have generated new interest in this potential pathway to hypertension. OBJECTIVES: To examine environmental factors associated with levels of circulating angiotensinogen as determinants of hypertension in populations of African origin. METHODS: We recruited 1557 participants from communities in Nigeria (n = 611), Zimbabwe (n = 161), Jamaica (n = 476), and Maywood, Illinois, USA (n = 309). RESULTS: Mean angiotensinogen levels varied widely across groups (Nigeria 1381 ng/ml angiotensin I generated, Zimbabwe 1638 ng/ml angiotensin and I generated Jamaica 1801 ng/ml angiotensin I generated, and Maywood 2039 ng/ml angiotensin I generated). Average body mass index was highly correlated to angiotensinogen level across the population samples, ...
Abstract: Association of Angiotensin Converting Enzyme Insertion/Deletion and Angiotensinogen T235 Polymorphisms with Risk of Essential Hypertension in Egyptian Patients
The Human Angiotensinogen ELISA uses two highly specific antibodies to measure angiotensin precursor levels in a variety of samples.
Synergistic effect of dexamethasone and isoproterenol on the expression of angiotensinogen in immortalized rat proximal tubular cells.
Complete information for AGT gene (Protein Coding), Angiotensinogen, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium
Reactome is pathway database which provides intuitive bioinformatics tools for the visualisation, interpretation and analysis of pathway knowledge.
The evolution of the understanding of the lung / alveolus in the last 30 years.. Old textbooks (circa 1970s) mostly offer hand drawings.. Since then, we have an improving understanding that has gone. from a view at the level of the microscope to the electron microscope. to the scanning electron microscope.. What is missing in the literature is giving the clinicians at bedside a. good understanding of the physics and physiology of the lung and the alveolus.. Ill give one example :. One of the major functions of the lung is an endocrine function : that of. converting Angiotensinogen to Angiotensin.. The lung is the primary place where ACE (angiotensinogen converting enzyme is. located. The kidney is the secondary place where ACE is found.. What happens to this pulmonary feature of conversion via enzymatic process in the. lung when the lung is significantly atelectatic or the lung is in serious crisis during. a pulmonary edematous event?. Angiotensin is the endogenous hormone that keeps ...
BioVendor - BioVendor Research and Diagnostic Products is a developer and manufacturer of immunoassays, recombinant proteins, antibodies and endotoxin-removal products.
B6.B6CB-Agt,tm1Afu,. Homozygous mutant mice do not produce angiotensinogen in the liver, resulting in the complete loss of plasma immunoreactive angiotensin I. The systolic blood pressure of the homozygous mutant is lower than wild-type, demonstrates an indispensable role for the renin-angiotensin system in maintaining blood pressure ...
A reverse haemolytic plaque assay (RHPA) for angiotensinogen was developed in rat hepatoma H4 cells and applied to investigate the possible secretion of angiotensinogen from rat pituitary cells in primary culture. Over a 24-hour incubation period in Cunningham chambers plaques with a mean area of 2,800 +/- 430 and 590 +/- 220 microns2/plaque (SD, n = 6) formed around all viable H4 cells and 2.8 +/- 0.59% of viable pituitary cells respectively. As a positive control PRL secretion from lactotrophs was routinely checked by the RHPA and shown to form plaques with a mean area of 4,050 +/- 1,850 microns2/plaque after a 4-hour incubation. By comparing plaque size in H4 cells with angiotensinogen release in cell culture, as quantified by radioimmunoassay, the secretion rate of angiotensinogen from pituitary cells was calculated as 22 +/- 8 ng/10(6) cells/24 h. Plaque-forming cells consisted of two morphologically distinct populations; 78% being small cells (less than 6 microns diameter) containing little
We identified candidate biomarkers for the prediction of the development of severe AKI, and the prognostic potential of the most promising candidate, angiotensinogen, was verified in a larger set of patients who developed AKI after cardiac surgery. We found that uAnCR was elevated in patients who developed more severe AKI after sample collection. Elevated uAnCR was associated with worsening of AKI, independent of changes in SCr and Cleveland Clinic score, and it was also associated with several secondary outcomes. The prognostic predictive power of uAnCR was improved when only patients who were classified as AKIN stage 1 at the time of sample collection were used in the analysis, indicating that angiotensinogen could be used to predict adverse outcomes among patients who have not yet developed severe AKI as measured by serum creatinine.. Our data suggest that angiotensinogen could be used at the time of diagnosis with AKI to assess the risk of adverse outcomes. This risk assessment could lead to ...
Progressive deterioration of renal function occurs during normal aging. Previous studies on the aging kidney have demonstrated glomerular hemodynamic changes, specifically, glomerular capillary hypertension, as maladaptations that lead to proteinuria and glomerular sclerosis over time. Aging rats treated with angiotensin-converting enzyme inhibition have relatively less proteinuria and sclerosis, suggesting that age-related changes in renal function may be associated with alterations in the intrarenal renin-angiotensin system, which thus may play a major role in the pathogenesis of these maladaptations. To investigate this possibility, renal and systemic renin-angiotensin systems were examined at an early phase of the aging process (3 months) and at a later phase (12 months) in male Sprague-Dawley rats. Although plasma renin and serum angiotensin-converting enzyme concentrations did not differ significantly, the intrarenal system showed down-regulation of renin mRNA and angiotensin-converting ...
PubMed journal article: Augmented circadian rhythm of the intrarenal renin-angiotensin systems in anti-thymocyte serum nephritis rats. Download Prime PubMed App to iPhone, iPad, or Android
Finnish physiologist Robert Tigerstedt and his assistant Per Bergman in 1858 observed that extracts from renal cortex of rabbits had a pressor effect upon intravenous injection. They named this substance renin, In 1958 the term "angiotensin" was given to active end product of the renin-angiotensin system by two research groups on arterial pressure, one in Indiapolis (USA) bh H Page and the other in Buenos Aires(Argentina) by Eduardo Braun Menendez. Αccording their results, the Argentina group, demonstrated that renin could act on a protein present in the plasma in order to release angiotenin (which at first was named "hypertensin"). This proteic substrate was named angiotensinogen as was the actual precursor of the active principle ...
Peptides , Fluorescent Labeled Peptides , Renin FRET Substrate I; DABCYL-GABA-Ile-His-Pro-Phe-His-Leu-Val-Ile-His-Thr-EDANS (also called Renin Substrate I in some literature) contains a renin cleavage site that occurs in the N-terminal peptide of human angiotensinogen. Cleavage of the substrate occurs specifically at the Leu-Val bond and corresponds to the renin cleavage site of angiotensinogen. This fluorogenic peptide substrate is used to continuously measure the proteolytic activity of human renin. The assay relies upon FRET-mediated, intramolecular fluorescence quenching that occurs in the intact peptide substrate. Efficient fluorescence quenching occurs as a result of favorable energetic overlap of the EDANS excited state and the DABCYL absorption, and the relatively long excited state lifetime of the EDANS fluorophore. Cleavage of the substrate by renin liberates the peptidyl-EDANS fragment from proximity with the DABCYL acceptor, restoring the fluorescence of the EDANS moiety. This leads to a
This study investigated the impact of catalase (Cat) overexpression in renal proximal tubule cells (RPTCs) on nuclear factor erythroid 2Crelated factor 2 (Nrf2) stimulation of angiotensinogen (or gene promoter, were also studied. from the renin-angiotensin program (RAS) have always been implicated in the advancement and development of diabetic nephropathy. Nevertheless, the root molecular mechanisms stay incompletely understood. As well as the systemic RAS, the life of an area intrarenal RAS in renal proximal tubule cells (RPTCs) continues to be well noted (1). Many lines of proof indicate that improved era of reactive air species (ROS) is normally central towards the advancement of hypertension and RPTC apoptosis in diabetes. ROS mediate high-glucose (HG) arousal of angiotensinogen (Agt; the only real precursor of most angiotensins) gene appearance in RPTCs in vitro (2C5). Transgenic (Tg) mice particularly overexpressing rat (r) Agt (rAgt) within their RPTCs develop hypertension and kidney ...
The renin-angiotensin system (RAS) is a hormone system that regulates blood pressure and extracellular volume in the body. The RAS sequentially processes angiotensinogen to angiotensin II (Ang II), a peptide hormone that is a potent vasoconstrictor. Inhibition of RAS components has been used successfully in the treatment of hypertension, heart failure and end organ damage. Renin catalyzes the first and rate-limiting step of the RAS cascade and renin is specific for angiotensinogen. Blockade of Ang II production by direct inhibition of renin has long been a therapeutic goal. Early renin inhibitors, such as enalkiren and remikiren, were effective in blood pressure lowering. However, due to poor oral bioavailability, duration of action, and high costs of synthesis, these early peptidomimetic inhibitors never progressed to pivotal clinical studies [1]. Continued clinical interest in renin has led to the recent approval of the first renin inhibitor, aliskiren (Tekturna™), a non-peptidic inhibitor ...
Исследование взаимосвязи аллельного полиморфизма генов ренин-ангиотензиновой системы, синтазы оксида азота и фолатного цикла с тяжестью ишемического инсульта
SCI de Taranan Uluslararası Dergilerdeki Makaleler:. 1. Fak AS, Küçükoğlu MS, Fak NA, Demir M, Ağır AA, Demirtaş M, Köse S, Ozdemir M. Expert panel on cost analysis of atrial fibrillation. Anadolu Kardiyol Derg. 2013 Feb;13(1):26-38. doi: 10.5152/akd.2013.004. Epub 2012 Oct 12. 2. Orun O, Nacar C, Cabadak H, Tiber PM, Doğan Y, Güneysel Ö, Fak AS, Kan B. Investigation of the association between dopamine D1 receptor gene polymorphisms and essential hypertension in a group of Turkish subjects. Clin Exp Hypertens. 2011;33(6):418-21. doi: 10.3109/10641963.2011.561898. Epub 2011 Jul 28.. 3. Cabadak H, Orun O, Nacar C, Dogan Y, Guneysel O, Fak AS, Kan B. The role of G protein β3 subunit polymorphisms C825T, C1429T, and G5177A in Turkish subjects with essential hypertension. Clin Exp Hypertens. 2011;33(3):202-8.. 4. Topal NP, Ozben B, Hancer VS, Tanrikulu AM, Diz-Kucukkaya R, Fak AS, Basaran Y, Yesildag O. Polymorphisms of the angiotensin-converting enzyme and angiotensinogen gene in ...
The activation of NMDA receptors that subsequently induce cell death is believed to be primarily caused by an influx of Ca2+ into the cells, which leads to the generation of free radicals.29 In addition, it has also been reported that an enhancement of the reactive oxygen species (ROS) production occurs after excessive increases in the intracellular free Ca2+ concentration.8 The predominant form of glutamate neurotoxicity that occurs in retinal tissues has been shown to be mediated by an overstimulation of the NMDA subtype of glutamate receptors. As a result, this causes an increase of the Ca2+ influx, which is then followed by cell death.6,30,31 Furthermore, in various eye diseases, such as retinal ischemia, glaucoma, diabetic retinopathy, and age-related macular degeneration, it has been proposed that glutamate excitotoxicity and oxidative stress contribute to the retinal damage that occurs in these disorders.32-34 An increase in the retinal angiotensinogen mRNA has also been found after ...
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The aim of this study was to demonstrate that hormonal vitamin D (calcitriol) modulates the local pancreatic islet renin-angiotensin system (RAS) whilst improving islet beta cell secretory function. I
Angiotensin, Renin, Angiotensin Ii, Prorenin, Bradykinin, Plasma, Renin-angiotensin System, Rats, Aldosterone, Inhibition, Blood, Tissue, Angiotensin I, Human, Patients, Blood Pressure, Pressure, Diabetes Mellitus, Endothelium, Angiotensinogen
Angiotensin is part of the renin-angiotensin-aldosterone system. It does not generally exist simply as angiotensin, but rather as angiotensinogen, befor...
Prorenin is a glycosylated aspartic protease that consists of 2?homologouslobes and is the precursor of renin. Renin activates the renin-angiotensinsystem by cleaving angiotensinogen, produced by the liver, to yield angiotensinI, which is further converted into angiotensin II by ACE, theangiotensin-converting enzyme primarily within the capillaries of the lungs. Ithas been reported that the levels of circulating prorenin (but not renin) areincreased in diabetic subjects.
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TY - JOUR. T1 - Modeling sex differences in the renin angiotensin system and the efficacy of antihypertensive therapies. AU - Leete, Jessica. AU - Gurley, Susan. AU - Layton, Anita T.. PY - 2018/4/6. Y1 - 2018/4/6. N2 - The renin angiotensin system is a major regulator of blood pressure and a target for many anti-hypertensive therapies; yet the efficacy of these treatments varies between the sexes. We use published data for systemic RAS hormones to build separate models for four groups of rats: male normotensive, male hypertensive, female normotensive, and female hypertensive rats. We found that plasma renin activity, angiotensinogen production rate, angiotensin converting enzyme activity, and neutral endopeptidase activity differ significantly among the four groups of rats. Model results indicate that angiotensin converting enzyme inhibitors and angiotensin receptor blockers induce similar percentage decreases in angiotensin I and II between groups, but substantially different absolute ...
ONLINE SUPPLEMENTAL MATERIAL Allele-Specific Expression of Angiotensinogen in Human Subcutaneous Adipose Tissue Sungmi Park 1, Ko-Ting Lu 1, Xuebo Liu 1, Tapan K. Chatterjee 2, Steven M. Rudich 3, Neal
This study provides preliminary evidence that a polymorphism in the AGT gene is independently associated with cerebral VR in white elderly persons. Homozygous carriers of the CC genotype of the rs699 SNPs have lower cerebral CO2 VR compared with the other genotypes.. To our knowledge, this is the first study to provide evidence that renin angiotensin system genes are also involved in cerebral VR. Previous evidence suggests a genetic role of this system in brain health and diseases such as stroke, depression, and cognitive impairment.26,27 This study adds evidence that this system may also be involved in VR, which is linked with aging outcomes such as stroke2 and dementia.28. CO2-dependent VR is mediated in part by the endothelium and is related to changes in nitric oxide.29,30 Changes in end-tidal CO2 are associated with fast changes in pH, which modulate the effect of nitric oxide synthase leading to changes in nitric oxide production.31 In addition, ATP-dependent K+ channel activation may ...
Abstract: The content of mRNA of renin-angiotensin system (RAS) genes in the kidney and heart of hypertensive ISIAH and normotensive WAG rats was measured by the real-time PCR. Statistically significant decrease of RAS gene mRNA was registered in the kidney of ISIAH rats, including Ren (by 45%), Аce (43%), АТ1А (34%), СОХ-2 (50%). In the myocardium АТ1А mRNA expression decreased by 28% while Ace mRNA expression increased by 80%. These results demonstrate the reduction of renal RAS basal activity in the hypertensive ISIAH rats, and this allows us to consider the ISIAH rat, as a low-renin hypertensive strain.In support of this viewpoint, in the ISIAH rats, a two-fold increase in the connective tissue sodium concentration as well as statistically significant plasma sodium increase (from 136±0,25 μmol/l in WAG to 139±0,3 μmol/l in the ISIAH rats) were found. Our conclusion backed by a tendency of the ISIAH plasma aldosterone level decrease giving in sum a classical picture of a ...
Principal Investigator:KOHZUKI Masahiro, Project Period (FY):1994 - 1995, Research Category:Grant-in-Aid for General Scientific Research (C), Research Field:Circulatory organs internal medicine
The results of the present study demonstrate the presence of increased concentrations of renin and prorenin in left ventricular tissue from patients with DCM. The cardiac levels of renin and prorenin were more than fivefold the cardiac levels in the donors. In addition, the cardiac tissue-to-plasma concentration ratios for renin and prorenin (molecular mass, 48 and 54 kD, respectively) were approximately threefold the ratio for serum albumin (molecular mass, 70 kD), indicating that the levels of renin and prorenin in cardiac tissue were too high to be explained by admixture with blood or by diffusion from the blood into the interstitial fluid. In normal porcine left ventricular tissue, the renin level was also higher than can be explained by its localization in extracellular fluid.4 Purified membrane fractions prepared from porcine left ventricular tissue contained renin,4 and specific binding of renin and prorenin to rat renal and other tissue membranes has been reported.35 36 In the present ...
Elevated oxidative stress is typical in the pathogenesis of heart failure. Characteristical changes in antioxidant enzyme status, represented by glutathionperoxidase (GSH-Px) and superoxide dismutase (SOD), and changes in heat shock protein status (Hsp), denoted by Hsp25 and Hsp72, have been revealed in two different rat-models. Lipidperoxidation was quantified by the concentration of thiobarbituric acid reactive substances (TBARS). In the first model of heart failure caused by permanent activation of renin-angiotensin system in double transgenic rat, leftventricular hypertrophy accompanied by a shift of creatine kinase (CK) isoenzyme pattern to higher concentration of fetale CK-MB an -BB-isoforms was found. Higher TBARS concentrations and lower alpha-tocopherol levels caused by consumption have been measured. SOD and Hsp72 remained unchanged. The tolerance against experimental hypoxia/reoxygenation was improved by higher levels of GSH-Px and Hsp25 in both right and left ventricular tissue. In ...
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Sigma-Aldrich offers abstracts and full-text articles by [Mohammad A K Azad, Jesmin Akter, Kelly L Rogers, Roger L Nation, Tony Velkov, Jian Li].
How is Quality Control Workstation (radiographic imaging system component) abbreviated? QCW stands for Quality Control Workstation (radiographic imaging system component). QCW is defined as Quality Control Workstation (radiographic imaging system component) rarely.
TY - JOUR. T1 - Irreversible Renal Damage after Transient Renin-Angiotensin System Stimulation: Involvement of an AT(1)-Receptor Mediated Immune Response. AU - Heijnen, Bart F. J.. AU - Nelissen, Jelly. AU - van Essen, Helma. AU - Fazzi, Gregorio E.. AU - Tervaert, Jan W. Cohen. AU - Peutz-Kootstra, Carine J.. AU - Mullins, John J.. AU - Schalkwijk, Casper G.. AU - Janssen, Ben J. A.. AU - Struijker-Boudier, Harry A. J.. PY - 2013/2/28. Y1 - 2013/2/28. U2 - 10.1371/journal.pone.0057815. DO - 10.1371/journal.pone.0057815. M3 - Article. VL - 8. JO - PLOS ONE. JF - PLOS ONE. SN - 1932-6203. IS - 2. M1 - e57815. ER - ...
The apelin-APJ system is a relatively new discovery. It has generated interest in part due to its apparent ability to counteract the renin-angiotensin system, which is frequently overactive in many cardiovascular disease.. Two of the main actions of apelin are to increase the pumping ability of the heart and cause blood vessels to relax. The investigators wish to assess if these actions are altered in the setting of normal renin-angiotensin activation and increased renin-angiotensin activity. ...
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Plasma renin then carries out the conversion of angiotensinogen, released by the liver, to angiotensin I.[2] Angiotensin I is ... Renin cleaves a decapeptide from angiotensinogen, a globular protein. The decapeptide is known as angiotensin I. ... angiotensinogen is picked up from the circulation or expressed locally in some tissues; with renin they form angiotensin I, and ...
Propeptides: Angiotensinogen. *Angiotensin I. Combinations:. *Valsartan/hydrochlorothiazide. *Valsartan/hydrochlorothiazide/ ...
... ogenEdit. Angiotensinogen (AGT) is an α-2-globulin produced constitutively and released into the circulation mainly ... Human angiotensinogen is 453 amino acids long, but other species have angiotensinogen of varying sizes. The first 12 amino ... Plasma angiotensinogen levels are increased by plasma corticosteroid, estrogen, thyroid hormone, and angiotensin II levels. ... Angiotensin I (CAS# 11128-99-7) is formed by the action of renin on angiotensinogen. Renin cleaves the peptide bond between the ...
"Interleukin-6 Mediates Angiotensinogen Gene Expression during Liver Regeneration". PLoS ONE. 8 (7): e67868. doi:10.1371/journal ... Dzau, VJ; Herrmann, HC (Feb 15-22, 1982). "Hormonal control of angiotensinogen production". Life Sciences. 30 (7-8): 577-84. ... Angiotensinogen expression Regenerate itself by hepatocyte mitosis Via STAT and Gab1: RAS/MAPK, PLC/IP3 and PI3K/FAK Cell ...
Sethi AA, Nordestgaard BG, Tybjaerg-Hansen A (July 2003). "Angiotensinogen gene polymorphism, plasma angiotensinogen, and risk ... Tanimoto K, Sugiyama F, Goto Y, Ishida J, Takimoto E, Yagami K, Fukamizu A, Murakami K (December 1994). "Angiotensinogen- ... Jeunemaitre X, Gimenez-Roqueplo AP, Célérier J, Corvol P (1999). "Angiotensinogen variants and human hypertension". Current ... Dickson ME, Sigmund CD (July 2006). "Genetic basis of hypertension: revisiting angiotensinogen". Hypertension. 48 (1): 14-20. ...
Dickson ME, Sigmund CD (July 2006). "Genetic basis of hypertension: revisiting angiotensinogen". Hypertension. 48 (1): 14-20. ...
One of these genes is the angiotensinogen (AGT) gene, studied extensively by Kim et al. They showed that increasing the number ... Dickson ME, Sigmund CD (July 2006). "Genetic basis of hypertension: revisiting angiotensinogen". Hypertension. 48 (1): 14-20. ...
"A redox switch in angiotensinogen modulates angiotensin release". Nature. 468 (7320): 108-11. doi:10.1038/nature09505. PMC ...
... s bind to the active site of renin and inhibit the binding of renin to angiotensinogen, which is the rate- ... Renin is a circulating enzyme that acts on a circulating peptide, angiotensinogen. Renin cleaves the peptide at the Leu10-Val11 ... Renin is highly selective for its only naturally occurring substrate which is angiotensinogen, and the incidence of unwanted ... The first generation of renin inhibitors, such as H-142, were peptide analogues of angiotensinogen. However, these inhibitors ...
"Kinetic studies of rat renin and tonin on purified rat angiotensinogen". Can. J. Biochem. Cell Biol. 62: 136-142. PMID 6097352 ...
February 1999). "Angiotensinogen gene polymorphisms M235T/T174M: no excess transmission to hypertensive Chinese". Hypertension ... It performs this function by breaking down (hydrolysing) angiotensinogen, secreted from the liver, into the peptide angiotensin ... angiotensinogen and epithelial sodium channel". Hypertension. 33 (6): 1324-31. doi:10.1161/01.hyp.33.6.1324. PMID 10373210. ...
2005). "Finb, a multiple zinc finger protein, represses transcription of the human angiotensinogen gene". Int. J. Mol. Med. 13 ...
Ricardo SD, Franzoni DF, Roesener CD, Crisman JM, Diamond JR (May 2000). "Angiotensinogen and AT(1) antisense inhibition of ...
Renin, a proteolytic enzyme, cleaves angiotensinogen to angiotensin I, which is converted to angiotensin II. In the case of ...
Human angiotensinogen is 453 amino acids long, but other species have angiotensinogen of varying sizes. The first 12 amino ... Angiotensinogen (AGT) is an α-2-globulin produced constitutively and released into the circulation mainly by the liver. It is a ... It is derived from the precursor molecule angiotensinogen, a serum globulin produced in the liver. It plays an important role ... Plasma angiotensinogen levels are increased by plasma corticosteroid, estrogen, thyroid hormone, and angiotensin II levels. ...
"Effect of Renin-Angiotensin System Blockade on the Expression of the Angiotensinogen Gene and Induction of Hypertrophy in Rat ... "Effect of renin-angiotensin system blockade on the expression of the angiotensinogen gene and induction of hypertrophy in rat ... "RAS blockade decreases blood pressure and proteinuria in transgenic mice over-expressing rat angiotensinogen gene in the kidney ... "Reactive oxygen species blockade and action of insulin on expression of angiotensinogen gene in proximal tubular cells". ...
... endothiapepsin and its complex with an angiotensinogen fragment analogue, H-142". Biochemical Society Transactions. 13 (6): ...
The protein catalyzes the final step in the conversion of angiotensinogen to angiotensin IV (AT4) and is also a receptor for ...
It cleaves angiotensinogen to angiotensin I, which is in turn converted by angiotensin-converting enzyme (ACE) to angiotensin ... Binding to this pocket prevents the conversion of angiotensinogen to angiotensin I. Aliskiren is also available as combination ...
Under normal physiological conditions, the enzyme renin converts angiotensinogen to angiotensin I, which will then be converted ...
Renin converts the inactive angiotensinogen into angiotensin I, which is converted to angiotensin II (AII) by angiotensin ...
Kushiki, K; Yamada H (2001). "Upregulation of Immunoreactive Angiotensin II Release and Angiotensinogen mRNA Expression by High ...
Binding of renin to this receptor induces the conversion of angiotensinogen to angiotensin I. This protein is associated with ...
Angiotensin II originates from plasmatic angiotensin I after the conversion of angiotensinogen by renin produced by the ... Angiotensin II originates from plasmatic angiotensin I after the conversion of angiotensinogen by renin produced by the ...
1995). "Identification of angiotensinogen and complement C3dg as novel proteins binding the proform of eosinophil major basic ... angiotensinogen (AGT), and C3dg. This protein may be involved in antiparasitic defense mechanisms as a cytotoxin and ...
title = "Hyperglycemia modulates angiotensinogen gene expression",. abstract = "Elevated plasma angiotensinogen (AGT) levels ... Hyperglycemia modulates angiotensinogen gene expression. Ilan Gabriely, Xiao Man Yang, Jane A. Cases, Xiao Hui Ma, Luciano ... Hyperglycemia modulates angiotensinogen gene expression. / Gabriely, Ilan; Yang, Xiao Man; Cases, Jane A.; Ma, Xiao Hui; ... N2 - Elevated plasma angiotensinogen (AGT) levels have been demonstrated in insulin-resistant states such as obesity and type 2 ...
RAS: renin-angiotensin system; AGT: angiotensinogen; REN: renin; AngI: angiotensin I; AngII: angiotensin II; Ang-(1-9): ... RAS: renin-angiotensin system; AGT: angiotensinogen; REN: renin; AngI: angiotensin I; AngII: angiotensin II; Ang-(1-9): ...
Angiotensinogen is expressed in an islet cell line (RIN 1056A) derived from a rat pancreatic tumor. Angiotensinogen mRNA ... Angiotensinogen is expressed in an islet cell line (RIN 1056A) derived from a rat pancreatic tumor. Angiotensinogen mRNA ... Angiotensinogen is expressed in an islet cell line (RIN 1056A) derived from a rat pancreatic tumor. Angiotensinogen mRNA ... Angiotensinogen is expressed in an islet cell line (RIN 1056A) derived from a rat pancreatic tumor. Angiotensinogen mRNA ...
Other plasma proteins may be increased (angiotensinogen/renin substrate, alpha-1-antitrypsin, ceruloplasmin). ...
Angiotensinogen di ubah menjadi angiotensin 1 dengan katalisis renin. Selanjutnya angiotensin… ... Angiotensin adalah hormone petida yang berasal dari protein angiotensinogen. ... Angiotensin adalah hormone petida yang berasal dari protein angiotensinogen. Angiotensinogen di ubah menjadi angiotensin 1 ...
Blood-borne angiotensin II is generated from angiotensinogen via cleavage by renin and angiotensin-converting enzyme (ACE), an ...
Angiotensinogen definition at Dictionary.com, a free online dictionary with pronunciation, synonyms and translation. Look it up ... angiotensinogen in Medicine Expand. angiotensinogen an·gi·o·ten·sin·o·gen (ānjē-ō-těn-sĭnə-jən). n. A serum globulin formed ...
High Molecular Weight Form Angiotensinogen Gene Renin System Renin Substrate Angiotensinogen mRNA These keywords were added by ... Gaillard I, Clauser E, Corvol P: Structure of human angiotensinogen gene. DNA1989, 8: 87 - 89.PubMedCrossRefGoogle Scholar ... Kimura S, Iwao H, Fukui K, Abe Y, Tanaka S Effect of thyroid hormone on angiotensinogen and renin mRNA levels in rat. Jpn J ... Ben-Ari ET, Garrison JC Regulation of angiotensinogen mRNA accumulation in rat hepatocytes. Am J Physiol 1988, 255:E70-E79 ...
... Natalia Ruggeri Barbaro, Vanessa Fontana, and Heitor Moreno ... angiotensinogen, and endothelial nitric oxide synthase genes," DNA and Cell Biology, vol. 30, no. 8, pp. 555-564, 2011. View at ... the main finding was the association of two genetic variants in the angiotensinogen (AGT) gene, the M allele of rs699 and the G ...
Urinary excretion of angiotensinogen reflects intrarenal angiotensinogen production.. Kobori H1, Harrison-Bernard LM, Navar LG. ... Urine levels of angiotensinogen after the treatment evaluated by radioimmunoassay were plotted against kidney (A) and plasma (B ... Urinary levels of angiotensinogen were highly correlated with kidney Ang II content, but not with the plasma Ang II level. ... The high salt (H/S) diet alone did not alter urinary angiotensinogen levels in sham animals (H/S + Sham; ); however, Ang II ...
The Human Angiotensinogen ELISA uses two highly specific antibodies to measure angiotensin precursor levels in a variety of ... Angiotensinogen Detection. Angiotensinogen (also known as serpin peptidase inhibitor, clade A, member 8; Serpin A8, Ang, Ang II ... Anti-Mouse/Rat Angiotensinogen (405) Rabbit IgG Affinity Purify 10 ug $125.00 ... Anti-Human Angiotensinogen (104AT 601.2.80) Mouse IgG MoAb 10 ug $126.00 ...
A1BG · AGC boxes · Angiotensinogen core promoter element · Boxes · cAMP response elements · B recognition elements · CAAT boxes ... A1BG/Quiz · AGC boxes/Quiz · Angiotensinogen core promoter element/Quiz · AP-1 box A and box B/Quiz · Pre-initiation complex ... Angiotensinogen[edit]. The diagram consists of spacefilling models of angiotensin I (left) and angiotensin II (right). Credit: ... Angiotensinogen core promoter element 1 (AGCE1) is an example of a core promoter element that may occur in a DNA sequence for ...
Buy our Recombinant Human Angiotensinogen protein. Ab191974 is a full length protein produced in HEK 293 cells and has been ... In response to lowered blood pressure, the enzyme renin cleaves angiotensinogen to produce angiotensin-1 (angiotensin 1-10). ...
Compare Angiotensinogen ELISA Kits from leading suppliers on Biocompare. View specifications, prices, citations, reviews, and ... Angiotensinogen ELISA Kits. The ELISA (enzyme-linked immunosorbent assay) is a widely used application for detecting and ...
AngiotensinogenAdd BLAST. 453. ,p>This subsection of the PTM / Processing section describes the position and length of an ... "A redox switch in angiotensinogen modulates angiotensin release.". Zhou A., Carrell R.W., Murphy M.P., Wei Z., Yan Y., Stanley ... IPR000227 Angiotensinogen. IPR023796 Serpin_dom. IPR000215 Serpin_fam. IPR036186 Serpin_sf. PANTHERi. PTHR11461 PTHR11461, 1 ... Angiotensinogen is present in the circulation in a near 40:60 ratio with the oxidized disulfide-bonded form, which ...
Angiotensinogen had the best discriminative characteristics. Urinary angiotensinogen was subsequently measured by ELISA and its ... Angiotensinogen / urine*. Biological Markers / urine. Female. Humans. Male. Middle Aged. Prognosis. Risk. Severity of Illness ... RESULTS: The urine angiotensinogen/creatinine ratio (uAnCR) predicted worsening of AKI, Acute Kidney Injury Network (AKIN) ... These data are the first to demonstrate the utility of angiotensinogen as a prognostic biomarker of AKI after cardiac surgery. ...
... the TT genotype of the angiotensinogen gene has been reported to be associated with a higher plasma level of angiotensinogen ... and genotype of the angiotensinogen gene (P=.2239, coefficient=−11.033 [TT=0, TM+MM=1]). The genotype of the angiotensinogen ... Angiotensinogen Gene and Blood Pressure in the Japanese Population. Naoharu Iwai, Hitoshi Shimoike, Nobuyuki Ohmichi, Masahiko ... Angiotensinogen Gene and Blood Pressure in the Japanese Population. Naoharu Iwai, Hitoshi Shimoike, Nobuyuki Ohmichi and ...
Angiotensinogen Gene Knockout Delays and Attenuates Cold-Induced Hypertension. Zhongjie Sun, Robert Cade, Zhonge Zhang, James ... Angiotensinogen Gene Knockout Delays and Attenuates Cold-Induced Hypertension. Zhongjie Sun, Robert Cade, Zhonge Zhang, James ... Angiotensinogen Gene Knockout Delays and Attenuates Cold-Induced Hypertension. Zhongjie Sun, Robert Cade, Zhonge Zhang, James ... Two groups of wild-type (WT) mice and 2 groups of angiotensinogen gene knockout (Agt-KO) mice (6 per group) were used. After ...
27 antibodies to Angiotensinogen and validated for use in 6 applications (Immunohistochemistry,Western Blot,Flow Cytometry, ... Angiotensinogen Antibodies The protein encoded by AGT, pre-angiotensinogen or angiotensinogen precursor, is expressed in the ... Angiotensinogen; angiotensinogen (PAT); angiotensinogen (serpin peptidase inhibitor, clade A, member 8); Des-Asp[1]-angiotensin ... II; pre-angiotensinogen; serine (or cysteine) proteinase inhibitor; Serpin A8; serpin peptidase inhibitor, clade A, member 8 ...
View our 6 Serpin A8/Angiotensinogen products for your research including Serpin A8/Angiotensinogen Proteome Profiler Antibody ... Serpin A8/Angiotensinogen: Products. The human serpin superfamily consists of at least 35 members that target not only serine ...
The angiotensinogen gene of Swiss mice is closely linked to a retrovirus-like element. Clouston, W.M. DNA Cell Biol. (1990) [ ... Influence of the angiotensinogen gene on the ovulatory capacity of mice. Hefler, L.A., Gregg, A.R. Fertil. Steril. (2001) [ ... Genetic control of fertility and embryonic waste in the mouse: A rolefor angiotensinogen. Tempfer, C.B., Moreno, R.M., Gregg, A ... Reduced angiotensinogen expression attenuates renal interstitial fibrosis in obstructive nephropathy in mice. Fern, R.J., Yesko ...
Renal Angiotensinogen Gene Expression and Tubular Atrophy in Diabetic Nephropathy , IntechOpen, Published on: 2012-04-20. ... Renal Angiotensinogen Gene Expression and Tubular Atrophy in Diabetic Nephropathy. By Brice E. T. Nouthe, Maya Saleh, Shao-Ling ...
Angiotensinogen and ACE mRNAs have been detected in normal cardiac tissue.10 11 12 13 Angiotensinogen mRNA is increased during ... Measurements of Angiotensinogen, ACE, and Serum Albumin. Angiotensinogen was measured as the maximum quantity of Ang I that was ... The lower ratio for angiotensinogen than for albumin may suggest that the angiotensinogen consumption rate, and therefore the ... when incubated with sheep angiotensinogen to be similar to the Vmax when incubated with angiotensinogen prepared from ...
Angiotensinogen Gene Promoter Region Variant Modifies Body Size-Ambulatory Blood Pressure Relations in Hypertension. Armindo D ... Angiotensinogen Gene Promoter Region Variant Modifies Body Size-Ambulatory Blood Pressure Relations in Hypertension ... Angiotensinogen Gene Promoter Region Variant Modifies Body Size-Ambulatory Blood Pressure Relations in Hypertension ... Angiotensinogen Gene Promoter Region Variant Modifies Body Size-Ambulatory Blood Pressure Relations in Hypertension ...
Metabolism of Angiotensinogen to Angiotensins (Homo sapiens). From WikiPathways. Revision as of 10:04, 11 June 2014 by ... After cleavage of angiotensinogen to angiotensin I by renin, two C-terminal amino acid residues of angiotensin I are removed by ... Angiotensinogen, a prohormone, is synthesized and secreted mainly by the liver but also from other tissues (reviewed in ... Haas E, Goldblatt H.; Kinetic constants of the human renin and human angiotensinogen reaction.; PubMed Europe PMC Scholia* ...
  • Angiotensinogen mRNA detected by Northern analysis is abundant in the cell line and is approximately 200 bases longer than the mRNA isolated from rat liver, due to both a longer poly(A) tract and the use of a second polyadenylation site. (utmb.edu)
  • Dexamethasone is a potent inducer of angiotensinogen mRNA, producing a progressive accumulation from 3 to 96 hr in culture (9-fold above control levels). (utmb.edu)
  • Immunocytochemical staining of pituitary cells after formation of plaques with anti-angiotensinogen, anti-LH and anti-PRL antiserum showed that the large plaque-forming cells were gonadotrophs and none were lactotrophs. (garvan.org.au)
  • The Human, Mouse, and Rat Total Angiotensinogen Assay Kits are ELISA kits that can be used to detect total or intact human, mouse or rat angiotensinogen in serum, EDTA-plasma, urine, or cell culture media. (clontech.com)
  • Human angiotensinogen has been purified 390-fold from serum by a rapid high-yielding procedure that involved chromatography on Blue Sepharose, phenyl-Sepharose, hydroxyapatite and immobilized 5-hydroxytryptamine (5-HT). (biochemj.org)
  • LS-F13066 is a 96-well enzyme-linked immunosorbent assay (ELISA) for the Quantitative detection of Human AGT / Angiotensinogen in samples of Plasma and Serum. (lsbio.com)
  • The plasma concentration of the placentally derived proMBP (proform of eosinophil major basic protein) increases in pregnancy, and three different complexes containing proMBP have been isolated from pregnancy plasma and serum: a 2:2 complex with the metalloproteinase, PAPP-A (pregnancy-associated plasma protein-A), a 2:2 complex with AGT (angiotensinogen) and a 2:2:2 complex with AGT and complement C3dg. (biochemj.org)
  • Rat angiotensinogen ELISA kit can be used for measuring quantitative levels of angiotensinogen in rat plasma, serum, cell culture supernatant and urine samples. (elisakits.co.uk)
  • It is derived from the precursor molecule angiotensinogen, a serum globulin produced in the liver . (wikipedia.org)
  • Therefore, the association of the insertion/deletion (I/D) polymorphism of the angiotensin converting enzyme (ACE) gene and the T235 (methionine to threonine substitution) polymorphism of the angiotensinogen (AGT) gene with intima-media thickness of the carotid artery was investigated. (uab.edu)
  • Common structural organization of the angiotensinogen and the α- 1 -antitrypsin genes . (springer.com)
  • Therefore, our objective was to determine whether the genes for placental renin (REN) and maternal angiotensinogen (AGT) interact to influence the risk of preeclampsia. (uib.no)
  • By comparing plaque size in H4 cells with angiotensinogen release in cell culture, as quantified by radioimmunoassay, the secretion rate of angiotensinogen from pituitary cells was calculated as 22 +/- 8 ng/10(6) cells/24 h. (garvan.org.au)
  • Urine levels of angiotensinogen after the treatment evaluated by radioimmunoassay were plotted against kidney ( A ) and plasma ( B ) Ang II levels. (nih.gov)
  • We investigated the detailed localization of angiotensinogen in 3 proximal tubule segments in the diabetic Otsuka Long-Evans Tokushima fatty (OLETF) rats and the control Long-Evans Tokushima Otsuka (LETO) rats. (ijbs.com)
  • Interestingly, the main finding was the association of two genetic variants in the angiotensinogen ( AGT ) gene, the M allele of rs699 and the G allele of rs5051, and TRH in white but not in African-American subjects. (hindawi.com)
  • Presence of the angiotensinogen (AGT) -6A allele or the AGT 235T allele were both associated with the most pronounced systolic BP response to atenolol treatment (P =.001 when -6 AA+AG was compared with GG and P =.008 for presence of the 235T variant compared with 235 MM). CONCLUSIONS: We found that SNPs in the angiotensinogen gene were associated with the BP lowering response to atenolol. (diva-portal.org)
  • The absorbance values of plasma angiotensinogen were significantly higher in the patients (0.71) with M235T allele than in the controls (0.53). (alliedacademies.org)