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.

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)

*Renin inhibitor

... 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 ...

*Essential hypertension

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. ...

*Biochemical cascade

"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 ...

*Serpin

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. ...

*African Society of Hypertension (AfSoH) Initiative

Dickson ME, Sigmund CD (July 2006). "Genetic basis of hypertension: revisiting angiotensinogen". Hypertension. 48 (1): 14-20. ...

*Randy Read

"A redox switch in angiotensinogen modulates angiotensin release". Nature. 468 (7320): 108-11. doi:10.1038/nature09505. PMC ...

*Renin-angiotensin system

Outside the liver, angiotensinogen is picked up from the circulation or expressed locally in some tissues; with renin they form ... Plasma renin then carries out the conversion of angiotensinogen, released by the liver, to angiotensin I. Angiotensin I is ... Renin cleaves a decapeptide from angiotensinogen, a globular protein. The decapeptide is known as angiotensin I. Angiotensin I ...

*Renal tissue kallikrein

"Kinetic studies of rat renin and tonin on purified rat angiotensinogen". Can. J. Biochem. Cell Biol. 62: 136-142. PMID 6097352 ...

*Pathophysiology of hypertension

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. ...

*RREB1

2005). "Finb, a multiple zinc finger protein, represses transcription of the human angiotensinogen gene". Int. J. Mol. Med. 13 ...

*Osteopontin

Ricardo SD, Franzoni DF, Roesener CD, Crisman JM, Diamond JR (May 2000). "Angiotensinogen and AT(1) antisense inhibition of ...

*Aortic insufficiency

Renin, a proteolytic enzyme, cleaves angiotensinogen to angiotensin I, which is converted to angiotensin II. In the case of ...

*Angiotensin

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. ...

*Serge Carrière

"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

... endothiapepsin and its complex with an angiotensinogen fragment analogue, H-142". Biochemical Society Transactions. 13 (6): ...

*Aliskiren

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 ...

*Penbutolol

Under normal physiological conditions, the enzyme renin converts angiotensinogen to angiotensin I, which will then be converted ...

*Fosinopril

Renin converts the inactive angiotensinogen into angiotensin I, which is converted to angiotensin II (AII) by angiotensin ...

*Forasartan

Kushiki, K; Yamada H (2001). "Upregulation of Immunoreactive Angiotensin II Release and Angiotensinogen mRNA Expression by High ...

*Leucyl/cystinyl aminopeptidase

The protein catalyzes the final step in the conversion of angiotensinogen to angiotensin IV (AT4) and is also a receptor for ...

*ATP6AP2

Binding of renin to this receptor induces the conversion of angiotensinogen to angiotensin I. This protein is associated with ...

*Adrenal cortex

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 ...

*Major basic protein

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 ...

*Pregnancy-associated plasma protein A

1995). "Identification of angiotensinogen and complement C3dg as novel proteins binding the proform of eosinophil major basic ...

*Subfornical organ

... participates in the control of body fluid homeostasis by regulating angiotensinogen gene transcription in the rat subfornical ...
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 ...
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 ...
We have previously shown that angiotensinogen, like other members of the serine protease inhibitor (serpins) family has anti-angiogenic properties in vitro on cultured endothelial cells and in ovo in the chick chorioallantoic membrane assay. By staining blood vessels of histological sections of the chick-chorioallantoic membrane with an endothelial-specific cell marker lectin we quantified vessel density in angiotensinogen treated areas and control areas: 48 hours after angiotensinogen was locally applied on the chick-chorioallantoic membrane we observed a 70% decrease in mesodermic vessel density in comparison to the control sections. Human angiotensinogen transfected chinese-hamster-ovary-cells grafted onto the surface of the chick-chorioallantoic membrane for 48 hours and constantly producing and secreting human angiotensinogen are leading to a similar decrease in vessel density of mesodermal blood vessels in comparison to non-transfected cells. As human angiotensinogen does not interact ...
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…
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
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Background: Angiotensin peptides may act locally as cytokines in several organ systems with elevated mucosal levels present in Crohns disease. A variant in the angiotensinogen gene promoter results in increased peptide production, while transforming growth factor β1 (TGFβ1) codon 25 variants demonstrate variable peptide production, predisposing to fibrosis in several organs.. Aims: Conduct an Australian-based analysis of the angiotensinogen-6 variant in two independent inflammatory bowel disease (IBD) cohorts, and examine the role of angiotensinogen-6 and TGFβ1 codon 25 variants in shaping Crohns disease phenotype.. Methods: IBD Patients (Crohns disease = 347, ulcerative colitis = 147) and CD families (n = 148) from two cohorts, together with 185 healthy controls were genotyped for angiotensinogen-6. Genotype-phenotype analyses were performed for both angiotensinogen-6 and TGFβ1 codon 25.. Results: Angiotensinogen-6 AA genotype was significantly associated with Crohns disease (p = 0.007, ...
Hypertension is a serious risk factor for myocardial infarction, heart failure, vascular disease, stroke, and renal failure. The renin-angiotensin system plays...
Complete information for AGT gene (Protein Coding), Angiotensinogen, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium
Most of renin-angiotensin system (RAS) gene polymorphisms have not yet been studied in the Iranian population. In the present study, the frequencies of common polymorphisms in the RAS genes, including angiotensin-converting enzyme (ACE) insertion/deletion (I/D) and three single-nucleotide polymorphisms (SNPs), i.e., A-240T, T-93C and A2350G, angiotensinogen M235T, angiotensin II receptor ...
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Angiotensin (Ang) II exaggerates cerebral injury in ischemic damage. Angiotensin-converting enzyme type 2 (ACE2) converts Ang II into Ang (1-7) and thus, may protect against the effects of Ang II. We hypothesized that neuronal ACE2 over-expression decreases ischemic stroke in mice with Ang II overproduction. Human renin and angiotensinogen double transgenic (RA) mice and RA mice with neuronal over-expression of ACE2 (SARA) were used for the study. The mean arterial pressure (MAP) was calculated from telemetry-recorded blood pressure (BP). SARA mice were infused peripherally with Norepinephrine 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 ...
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
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 ...
Define pepsitensin: a vasoconstrictor pressor polypeptide similar to angiotensin formed by the action of pepsin on angiotensinogen
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...
Evidence has accumulated to support the concept that the kidney is a major reservoir for a complete and independent RAS. Pioneering work in this area was done by Navar et al. (36), who demonstrated the intrarenal formation of ANG II. Subsequently, Anderson et al. (1) characterized the expression of angiotensinogen and ACE in diabetic rat kidneys. Furthermore, membrane-bound ACE has been found to reside in proximal tubular cells (26, 33, 51). In fact, the luminal concentration of ANG II at the level of the proximal tubule is ∼1,000-fold higher than the plasma concentration (25) by virtue of local ACE activity. Although evidence for an intratubular RAS appears solid, functional evidence for an intraglomerular RAS is somewhat less definitive. In a model of streptozotocin-induced diabetic rats, Singh et al. (49) demonstrated increased ANG II and renin content from glomerular extracts. Other studies have attempted to implicate specific cell types within the glomerulus and found that mesangial cells ...
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For comparison of the baseline characteristics, between-group data were compared with the Students unpaired t test for continuous data and the χ2 test for categorical data. With regard to the 6 polymorphisms within the AGT gene, because they were located on the same chromosome with short distances between each other, they probably did not segregate independently and had linkage disequilibrium (LD) between each other.25 Therefore, we first used haplotype analysis for these 6 polymorphisms to determine whether there were any specific haplotypes that were associated with AF. The methods of the expectation-maximization-based haplotype frequency estimation and permutation-based hypothesis-testing procedure were performed on the basis of the work of Fallin et al.27 After we obtained a significant haplotype profile analysis,27 we performed the individual haplotype analyses27 and single-locus analyses with multiple test correction for the probability value.. For single-locus analyses, allele ...
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 ...
The purpose of this study was to evaluate the relationship between angiotensin-converting enzyme (ACE; insertion/deletion), angiotensinogen (AGT M235T), and angiotensin II type 1 receptor (AT1R 1166A|C) and the prevalence of primary ovarian insuffici
The UBR (University of Brighton Repository) is a central institutional repository that records the work of the Universitys researchers. It is an open access, organic resource and is freely available via the web to researchers worldwide.
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 ...
We investigated whether angiotensin (ANG) II and its receptors contribute to lipopolysaccharide (LPS)-induced microglial activation through activation of the proinflammatory transcription factors nuclear factor κB (NF-κB) and activator protein-1 (AP-1). Using primary microglial cell cultures, we examined whether losartan [ANG type 1 receptor (AT1) antagonist] alters the effects of LPS on: the production of interleukin-1 (IL-1) and nitric oxide, cell morphology, and NF-κB and AP-1 activities. Reverse transcription-polymerase chain reaction revealed that LPS-stimulated microglial cells exhibited marked mRNA expression for AT1, ANG type 2 receptor (AT2) and the ANG II precursor angiotensinogen, whereas non-stimulated microglial cells expressed only those for AT2 and angiotensinogen. We further demonstrated marked peptide/protein expression for AT1 and ANG II in LPS-activated microglial cells. LPS (100 ng/mL)-stimulated microglial cells showed increased concentrations of IL-1 and nitrite (a ...
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].
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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The kidney is an organ in our body that resembles like bean. This organ performs several essential functions to save our body from the various diseases; this organ also serves as natural filter of the blood. Kidney is a very important organ of the body because it is responsible for the re-absorption of water, glucose Read more ...
This study will enroll the patients who have completed protocol AGT-181-102 where the patient, sponsor and investigator believe the patient may potentially benefit by continuing to receive AGT-181. Patients who enter the trial from early cohorts (for example 1 mg/kg) will continue on their assigned dose from the prior study until safety from the highest dose cohort is assessed. After safety and tolerability of the highest dose is known, patients may have their dose changed. ...
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LaborChemie findet durch technische Beratung die passende Lösung. Wir sind tätig im Bereich der Partikelmessung, OnLine Analytik, Spektroskopie, und Chemometrie, Strömungspotenzialmessung.
... ist eine ausosomal rezessive Erkrankung, die durch Mutationen im Gen C3 gekennzeichnet ist und kann zu verschiedenen immunologischen Störungen führen kann, insbesondere Störungen der Abwehr von bekteriellen Infektionen.. ...
Das MVK-gen kodiert die Mevalonatkinase ein Schlüsselenzym bei der Synthese der Sterole. Mutationen führen zu verschiedenen dominanten oder Rezessiven Erkrankungen, die vor allem durch eine gestörte Regulation der Entzündungsprozesse gekennzeichnet sind.. ...
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OBJECTIVE The term "receptor-associated prorenin system" (RAPS) refers to the pathogenic mechanisms whereby prorenin binding to its receptor dually activates the tissue renin-angiotensin system (RAS) and RAS-independent intracellular signaling via the receptor. The aim of the present study was to define the association of the RAPS with diabetes-induced retinal inflammation.. RESEARCH DESIGN AND METHODS Long-Evans rats, C57BL/6 mice, and angiotensin II type 1 receptor (AT1-R)-deficient mice with streptozotocin-induced diabetes were treated with (pro)renin receptor blocker (PRRB). Retinal mRNA expression of prorenin and the (pro)renin receptor was examined by quantitative RT-PCR. Leukocyte adhesion to the retinal vasculature was evaluated with a concanavalin A lectin perfusion-labeling technique. Retinal protein levels of vascular endothelial growth factor (VEGF) and intercellular adhesion molecule (ICAM)-1 were examined by ELISA. Retinal extracellular signal-regulated kinase (ERK) activation was ...
Persons with hypertension (HTN) often have higher uric acid than normotensives, especially in hypertensives with metabolic syndrome.1-5 Recent prospective studies also suggest that persons with higher uric acid are at greater risk to develop hypertension.4-7 Uric acid in childhood appears to be particularly predictive of both early-onset hypertension and blood pressure later in life.4, 5, 8 While many had considered elevated uric acid as merely a marker for increased renal sodium reabsorption, recent data suggests a potentially causal role. Rats made mildly hyperuricemic by treatment with the uricase inhibitor oxonic acid become hypertensive. The increase in blood pressure in these rats was blocked by administration of renin-angiotensin system (RAS) blockers or by reduction of uric acid with allopurinol.9 More recently, febuxostat was also shown effective in this experimental model.10 Febuxostat was recently approved by the FDA as Uloric. Febuxostat is a xanthine oxidase (XO) inhibitor (like the ...
http://youtu.be/iAZmLkSCmY0 GIMA AMEZIA SARI G1F011016 DESKRIPSI Renin adalah enzim dengan protein kecil yang dilepaskan oleh ginjal bila tekanan arteri turun sangat rendah. Pengeluaran renin dapat disebabkan aktivasi saraf simpatis (pengaktifannya melalui β1-adrenoceptor) (Guyton dan Hall,1997). Angiotensin adalah hormone petida yang berasal dari protein angiotensinogen. Angiotensinogen di ubah menjadi angiotensin 1 dengan katalisis renin. Selanjutnya angiotensin…
Figure 3. Cytokines and end-organ dysfunction in hypertension. A, In vessels, T cells infiltrate the adventitia and perivascular fat through the vasa vasorum. T cell-derived interleukin (IL)-17A acts on smooth muscle cells and adventitial fibroblasts to increase endothelial nitric oxide synthase (eNOS) phosphorylation, reactive oxygen species (ROS) production, collagen synthesis, and chemokine production, leading to a decrease in bioavailable nitric oxide (NO) and impaired vasodilation, increased vascular stiffness, and increased recruitment of immune cells, propagating the inflammatory response. These effects result in vascular dysfunction. B, In the renal medulla and cortex, activated T cells produce cytokines, such as IL-6 and interferon (IFN)γ that stimulate production of angiotensinogen. Angiotensinogen is converted to angiotensin I (Ang I) by intrarenal renin and subsequently to angiotensin II (Ang II) by intrarenal angiotensin-converting enzyme. Angiotensin II upregulates and stimulates ...
Am J Physiol Renal Physiol. 2004 May;286(5):F965-71. Epub 2004 Jan 13. Research Support, Non-U.S. Govt; Research Support, U.S. Govt, P.H.S.
American Journal of Physiology - Regulatory, Integrative and Comparative Physiology® and the APS® logo are registered trademarks of the American Physiological Society , Print ISSN: 0363-6119 , Online ISSN: 1522-1490. ...
We performed a large, long-term cohort study to evaluate the association of renin-angiotensin-aldosterone system gene polymorphisms and baseline phenotypes to all-cause mortality among individuals with angiographically confirmed coronary atherosclerosis. higher long-term all-cause mortality, actually after correcting for founded cardiovascular risk factors. As a complex, multifactorial disease that is affected by multiple pathophysiologic, genetic, and environmental factors, atherosclerotic cardiovascular disease (CVD) Pdpn is definitely a major health burden worldwide1,2,3. In addition to additional well-recognized risk factors, the renin-angiotensin-aldosterone system (RAAS) has been implicated in the development of atherosclerosis and coronary heart disease4. The RAAS regulates blood pressure, the sodium and water. Continue Reading. ...
Altogether the inhibitory serpins make up some 10% in molar terms, of the proteins in human plasma. Also present, in plasma, though in smaller concentrations, are other serpins that have lost their inhibitory activity but have taken on other functions vital to life; examples are the vasopressor peptide source angiotensinogen, and the thyroxine and corticosteroid binding globulins, TBG and CBG. The reason for the evolutionary success of the serpins is their possession, uniquely amongst the many families of serine protease inhibitors, of a mobile reactive site loop. It is the ability of this loop to profoundly change its conformation that enables the serpins to bind to their target proteases as a virtually irreversible complex. ...
A method is described for estimating plasma renin activity by using renin substrate present in plasma. This method differs from other indirect renin assay methods by (1) incubation in the absence of ions thus establishing conditions for zero order kinetics for the reaction between endogeneous renin and substrate and (2) the use of angiotensinase inhibitors di-sodium ethylenediamine tetraacetic acid (EDTA) and d-isopropylfluorophosphate (DFP). Recoveries of renin added to plasma in levels similar to those occurring in plasma are 85% SD±7%.. The incubation was done at pH 5.5 which was shown to be the optimum for human renin reacting with human substrate.. By incubating human plasma samples with known quantities of human renin, evidence was obtained suggesting that factors other than enzyme or total substrate concentrations affect the velocity of angiotensin formation. This variability of reaction rate may be explained by the existence of an inhibitor or activator in this system or by a variation ...
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YAO Li , KOBORI Hiroyuki , RAHMAN Matlubur , SETH Dale M. , SHOKOJI Takatomi , FAN Yuyan , ZHANG Guo-Xing , KIMURA Shoji , ABE Youichi , NISHIYAMA Akira Hypertension research : clinical and experimental : official journal of the Japanese Society of Hypertension 27(7), 493-500, 2004-07-01 医中誌Web 参考文献43件 被引用文献13件 ...
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AGT International to Share Urban Management Best Practice Insights with Chinas Mayors Over 50 of Chinas Leading Mayors to Participate in AGT Seminar -
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Post-transplant hypertension is a common occurrence during treatment with calcineurin inhibitors (CNIs) in kidney transplant population. The pathogenesis of vasoconstriction induced by CNIs involves vascular tone alterations and kidney sodium transport regulation. Among the factors involved a key role is played by the activation of intrarenal renin-angiotensin system with enhanced release of Angiotensin II (Ang II) and increase of oxidative stress. A common pathway between oxidative stress and hypertension induced by CNIs may be identified in the involvement of the activation of RhoA/Rho kinase pathway, key for the induction of hypertension and cardiovascular-renal remodeling, of the oxidative stress mediated increased nitric oxide (NO) metabolism and increased renal sodium retention via increased activity of thiazide-sensitive sodium chloride cotransporter (NCC) in the distal tubule ...
Open Session for UI faculty, research scientists and research assistants):. -- Rhinda Goedken: Drawbacks of GENEHUNTER for Larger Pedigrees: Application to Panic Disorder.. -- Brenda Sorensen: Calcium-dependent Melittin Binding to Paramecium Calmodulin is Domain- Specific and Altered by Mutations. College of Medicine Graduate Student Poster Presentation Awards:. -- Branimir Cvetkovic: Molecular and Physiological Analysis of Human Angiotensinogen Variants in vivo and Their Impact on Blood Pressure Phenotype.. -- Jennifer Edwards: Complement Receptor Type 3 (CR3) on Primary Human Cervical Cells Mediates Neisseria gonorrhoeae-induced Membrane Ruffling and Cellular Invasion.. -- Emily Kuhn: Insulators: Structural Components of Chromosomes or Transcriptional Regulators?. -- Lei Liu: Disruption of DEG/EnaC Proteins Resulted in Salt Taste Defect in Drosophila Melanogaster.. -- Robert Walters: Binding of Adeno-associated Virus Type 5 to 2,3-Linked Sialic Acid is Required for Gene ...
Peptides , Angiotensins and Related Peptides , Peptide Substrate for Renin 520 Assay kit; This FRET peptide is a specific substrate for renin. Aspartyl protease cleaves angiotensinogen to yield angiotensin I, which is further converted to angiotensin II. The renin-angiotensin system is a coordinated hormonal cascade in the control of cardiovascular, renal, and adrenal function. It governs body fluid and electrolyte balance, as well as arterial pressure. Since an overactive renin-angiotensin system leads to hypertension, renin is an attractive target for the treatment of this disease. This renin peptide substrate may be used for screening of renin inhibitors. In the FRET peptide, the fluorescence of 5-FAM is quenched by QXL 520. Upon cleavage into two separate fragments by renin, the fluorescence of 5-FAM is recovered, and can be monitored at excitation/emission = 490/520 nm. This substrate is employed in the SensoLyte 520 Renin Assay Kit, cat # 72040.
Renin produced by the kidney in response to glomerular hypoperfusion cata-lyzes cleavage of angiotensinogen (produced by the liver) to angiotensin (AT), which in turn is cleaved by angiotensin-converting enzyme (ACE) to angiotensin II, which acts on two receptors. The AT1 receptor mediates the vasoconstrictor effects of AT. The actions of the AT2 receptor are less well defined.. Angiotensin-converting enzyme inhibitors Mechanism of action. These drugs inhibit the conversion of angiotensin I to angiotensin II and. reduce angiotensin II mediated vasoconstriction.. Indications. The main indicators are heart failure, hypertension, diabetic nephropathy and ischaemic heart disease.. Preparations and dose. Perindopril. Tablets: 2 mg, 4 mg, 8 mg.. ■ Hypertension, initially 4 mg once daily (use 2 mg if in addition to diuretic, in the elderly, in renal impairment) subsequently adjusted according to response to maximum 8 mg daily. ■ Heart failure: initially 2 mg once daily, increased after at least 2 ...
Introduction. Essential hypertension (EH) is a multifactorial disease triggered by several genetic and multiple environmental factors in conjunct. Epidemiological studies have suggested that genetic variants, including those of the genes for angiotensinogen (AGT)1, renin (REN)2, angiotensin-converting enzyme (ACE)3, angiotensin II receptor type 1 (AGTR1)4,5, and aldosterone synthase (CYP11B2)6 increase the risk for EH. However, the influence of polymorphic forms of these genes has shown conflicting results in different populations7,8. This scenario might be reflecting the variable impact of the genetic background of populations and the interaction of environmental factors, which, in turn, might be modulating this molecular background. Recent literature data have shown that unfavorable genotype/allele alone might indicate a minor or nonsignificant association with EH. However, the co-occurrence of different unfavorable genotypes and clinical risk factors can increase the risk of hypertension. ...
BULGULAR: CBM grubunun RENIN, anjiotensinojen (ANGTS), ve anjiotensin d n t r c enzim-I (ACE I) mRNA ekspresyon d zeyleri miyelom hastalar ndan anlaml olarak y ksek idi (s ras yla, p=0,03, p=0,002, ve p=0,0008). Sa l kl allojeneik don rlerin CD34+ k k h cre rneklerindeki RENIN ve ANGTS mRNA ekspresyon d zeyleri myelom hastalar n n k k h cre rneklerinden anlaml derecede y ksek bulundu (p=0,001 and p=0,01). Bununla birlikte, CD34+CBM ve CD34+MM hematopoetik h crelerde ACE I ekspresyon d zeyleri aras nda anlaml fark g zlenmedi (p=0,89 ...
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Background It is not known whether drugs that block the renin-angiotensin system reduce the risk of diabetes and cardiovascular events in patients with impaired .... ...
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Enter patient details into monitor. • Choose non-dominant arm. • Select appropriate cuff. • Select frequency of measurement - usually every 30 min day and night. • Inactivate measurement display. • Give patient oral and written instructions and a diary card. • Instruct patient to carry on normal activities. • Instruct patient on how to remove and inactivate monitor after 25 h. • Allow 25 h recording so as to obtain full 24 h. • Daytime minimum - 20 measurements of systolic and diastolic blood pressure. Other associations Angiotensinogen gene may be related to hypertension Angiotensin converting enzyme gene may be related to left ventricular hypertrophy or hypertensive nephropathy α-Adducin gene may be related to salt-sensitive hypertension Autosomal dominant polycystic kidney disease (PKD-1 and PKD-2): a primary renal disease that frequently causes hypertension Salt sensitivity is likely to be distributed in a Gaussian or normal distribution rather than a dichotomous ...
Definition : Immunoassay reagents intended to perform qualitative and/or quantitative analyses on a body fluid sample (e.g., serum) to determine the level of one or both of the vasopressor hormones angiotensin I and/or angiotensin II. Angiotensin I, a decapeptide, is produced in the blood by the hydrolization of angiotensinogen (previously produced in the liver) by renin; it is rapidly converted into angiotensin II, an octapeptide, by a circulating angiotensin-converting enzyme. Angiotensin II is a powerful vasoconstrictor that also stimulates the cells of the zona glomerulosa to produce aldosterone.. Entry Terms : "Peptidyl-Dipeptidase A Determination Reagents" , "Angiotensin I/II Determination Reagents" , "Reagents, Immunoassay, Renal Metabolism, Angiotensin I/II". UMDC code : 19879 ...
All the classic components of the RAS (renin, angiotensinogen, ACE, and Ang-II type 1 and 2 receptors) have been identified in the pancreas, where they are thought to modulate β-cell function (3,4). Several studies implicate RAS overactivity in the development of islet dysfunction (8,10). Notably, in vitro (22.2 mmol/l glucose) and genetic (Zucker diabetic fatty rat) models of type 2 diabetes show increased expression of ACE and AT1R in islets, supporting the idea of a feed-forward mechanism ultimately resulting in β-cell dysfunction (7,10). While ACE2 has been shown to be elevated in renal tubules and cortex of db/db mice, prior to the onset of diabetic nephropathy (22), its relationship with β-cell function has not been studied. Our study shows the following: 1) islet ACE2 expression is upregulated at 8 weeks and tends to be reduced at 16 weeks of age in db/db mice islets compared with db/m controls; 2) Ad-hACE2-eGFP significantly increased ACE2 expression and activity in the mouse ...
ATRAP (angiotensin II type 1 receptor-associated protein) is a molecule which directly interacts with AT1R and inhibits AT1R signaling. The aim of this study was to examine the effects of continuous angiotensin II (ANG II) infusion on the intrarenal expression and distribution of ATRAP, and to determine the role of AT1R signaling in mediating these effects. C57BL/6 male mice were subjected to vehicle or ANG II infusions at doses of 200, 1000, or 2500 ng/kg/min for 14 days. ANG II infusion caused significant suppression of ATRAP expression in the kidney, but did not affect ATRAP expression in the testis or liver. Although only the highest ANG II dose (2500 ng/kg/min) provoked renal pathological responses, such as an increase in the mRNA expression of angiotensinogen and α−subunit of the epithelial sodium channel, ANG II-induced decreases in ATRAP were observed even at the lowest dose (200 ng/kg/min), particularly in the outer medulla of the kidney, based on immunohistochemical staining and ...
Recently developed molecular biology techniques lend themselves to the study of both normal physiology and pathophysiology. This review discusses a number of such techniques and their applicability to the study of diabetes and hypertension with the renin-angiotensin system as an example. The demonstration of specific mRNA in tissue provides strong evidence that the protein for which it encodes is expressed there. The contribution of several methods to demonstrate mRNA expression including Northern analysis, slot blot analysis, solution hybridization, in situ hybridization, run-on assays, and polymerase chain reaction are discussed in the light of how these are used to study renin-angiotensin system mechanisms. Additionally, recent developments in the study of gene transfer and identification of genes are reviewed.. ...
1. A synthetic 3-([14C]valine)-labelled tetradecapeptide renin substrate was used to measure renin concentration. Renin liberated 14C-labelled angiotensin I, which was separated from the labelled substrate by paper chromatography. The conversion of substrate into angiotensin I was quantitated by liquid-scintillation counting of radioactivity. 2. The rate of conversion of the substrate into angiotensin I was shown to be linearly related to renin concentration and time under suitable conditions. Angiotensin generation measured in this system agrees well with that measured by bioassay. 3. It is suggested that the use of a pure substrate offers advantages that include the standardization of current units of renin measurement.. ...
Russo, J., Balogh, G.A., Chen, J.Q., Fernandez, S.V., Fernbaugh, R., Heulings, R., Mailo, D.A., Moral, R., Russo, P.A., Sheriff, F., Vanegas, J.E., Wang, R., Russo, I.H., 2006, The concept of stem cell in the mammary gland and its implication in morphogenesis, cancer and prevention. Front Biosci 11, 151-172.PubMedGoogle Scholar ...
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Experimental data indicate the existence of a vascular tissue renin-angiotensin system in several different vessels from various animal models. Active renin can be locally synthesized into the vessel wall or taken up from circulating plasma to produce vascular angiotensin II. Using the human forearm technique, we produced evidence indicating the release of active and inactive renin and of angiotensin II from the vessels of hypertensive patients. Moreover, the production of vascular angiotensin II seems to be strictly correlated to the circulating renin profile, suggesting the possibility that vascular renin might be at least partially taken up from plasma. To investigate a possible function of the vascular renin-angiotensin system, we studied its interaction with sympathetic neurotransmission in essential hypertensive patients. In line with animal studies, vascular angiotensin II increases the vasoconstriction induced by the stimulation of the sympathetic nervous system through the potentiation ...
The human pancreas has vital roles in the regulation of glucose homeostasis and digestion and its dysfunction leads to pancreatic disease as diabetes and pancreatitis. Recent researches have highlighted the novel roles of a local renin-angiotensin system (RAS) in the pancreas and its clinical relevances; its inapprporiate activation leads to pancreatic endocrine and exocrine disease, notably type 2 diabetes. As such, manipulation of the overactive RAS may improve pancreatic islet cell function, cell mass and insulin sensitivity, as well as enhancing the growth and differentiation of pancreatic stem cells. Blockade of the RAS may be protective against pancreatitis and pancreatic cancer. The research outcome of current progress on the RAS in the pancreas should provide an alternative approach to preventing and treating, as well as curing pancreatic disease. This book discusses the progress of research on the renin-angiotensin system in the pancreas from the science to the bedside, providing a ...
Renin catalyzes the first step in the activation pathway of angiotensinogen--a cascade that can result in aldosterone release,vasoconstriction, and increase in blood pressure. Renin, an aspartyl protease, cleaves angiotensinogen to form angiotensin I, which is converted to angiotensin II by angiotensin I converting enzyme, an important regulator of blood pressure and electrolyte balance. Transcript variants that encode different protein isoforms and that arise from alternative splicing and the use of alternative promoters have been described, but their full-length nature has not been determined. Mutations in this gene have been shown to cause familial hyperproreninemia. [provided by RefSeq, Jul 2008 ...
Daniela Ravizzoni Dartora, Université de Montréal. Supervisor: Anne Monique Nuyt, Université de Montréal. Nearly 10% of Canadian children are born preterm each year. Improvements in neonatal intensive care have resulted in survival of the vast majority of these infants. Preterm birth results in ex utero development of an immature cardiovascular system. Studies now support a direct causal association between preterm birth and adverse changes in cardiovascular structure and function, which persist into adulthood, and are associated with hypertension, metabolic disorders and stroke. Clinical and experimental studies have shown how preterm birth and the pro- inflammatory and pro-oxidative nature of its related conditions (such as O2 toxicity), contribute to altered cardiac development (hypertrophy, fibrosis), vascular dysfunction, defective vascular growth with small vessels rarefaction and activation of the renin-angiotensin system (RAS) which are all involved in the programming of hypertension ...
angiotomy, angiotensinogen, angiotensin, angiotelectasia, angiostomous, angiostenosis, angiostaxis, angioscotometry, angioscotoma, angioscopy, angiosarcoma, angiorraphy, angiopoiesis, angioplasty, angiophacomatos, angiopathy, angioparesis, angioparalysis, angiomyoma, angiomegaly, angiomatous, angiomatosis, angiolysis, angiology, angiolith, angiokeratosis, angiod, angiohyalinosis, angiography, angiogram, angiogenin, angiogenesis, angioedema, angiodystrophy, angiodysplasia, angiocarpous ...
Obesity is a major health problem worldwide; it is associated with more than 30 medical conditions and is a leading cause of unnecessary deaths. Adipose tissue not only acts as an energy store, but also behaves like an endocrine organ, synthesising and secreting numerous hormones and cytokines. Angiotensin II (ANG II) is the biologically active component of the renin-angiotensin system (RAS). The RAS is present in adipose tissue and evidence suggests that ANG II is intimately linked to obesity. Indeed, ANG II increases fat cell growth and differentiation, increases synthesis, uptake and storage of fatty acids and triglycerides and possibly inhibits lipolysis. Evidence obtained using genetically modified animals has shown that the amount of body fat is directly related to the amount of ANG II, i.e., animals with low levels of ANG II have reduced fat stores while animals with excessive ANG II have increased fat stores. In humans, epidemiological evidence has shown that body fat is correlated with ...
Diabetic nephropathy (DN) is a leading cause of end-stage renal disease in developed countries where type 2 diabetes mellitus has reached epidemic proportions. Although the exact pathogenesis of DN is not fully understood and is likely diverse in nature, there are convincing data that the renin-angiotensin system (RAS) is a major mediator of renal injury. Angiotensin II (Ang II), traditionally playing a central role as a mediator of glomerular hemodynamic adaptation and injury, is now recognized to exert proinflammatory action leading to upregulation of chemokines, adhesion molecules, and other fibrogenic growth factors that culminate in a decline of renal function. Hyperglycemia and mechanical stress deriving from glomerular hypertension are the key factors underlying pathogenesis of DN. The common signaling pathways stimulated by high glucose and mechanical insult may act synergistically, thereby accelerating the cell damage. Podocytes are subjected not only to the load of filtered glucose but ...
Description: The significant impact of the renin-angiotensin system (RAS) on basic research and its clinical relevance are reflected by the flourishing publication of original and review research articles; by the appearance of whole issues of journals dedicated to the RAS; and by specialist books on the RAS. In such a rapidly evolving environment, publications that span the spectrum from basic research to the bedside, fill a particularly valuable niche for clinicians and researchers alike. The primary aim of this book is to provide a topical and timely forum for the critical appraisal of an area of RAS research that is expanding rapidly. In this respect, a collection of thirteen chapters from distinguished and world-class experts in the field has been presented on the contemporary research of the RAS and their implications in human disease. It is clear that outstanding and stellar work on the novel roles of local RAS and their potential clinical application is being done in laboratories and ...
A Genetic Variant in the Distal Enhancer Region of the Human Renin Gene Affects Renin Expression. . Biblioteca virtual para leer y descargar libros, documentos, trabajos y tesis universitarias en PDF. Material universiario, documentación y tareas realizadas por universitarios en nuestra biblioteca. Para descargar gratis y para leer online.
Es gibt nicht ausreichend Adjektive, um zu beschreiben was ich beim Anhören von „Substanz(-ver)lust" denke und fühle. Als erstes kamen mir in den Sinn: Absonderlich, verquer, grotesk. Die Liste ließe sich endlos fortführen. „Substanz(-ver)lust" ist einfach zutiefst schräge und bizarre Musik. Hier irgendeine Schublade aufzureißen ist ein hoffnungsloses, weil zum Scheitern verurteiltes Unterfangen. Kategorien sind scheiße, deshalb wird einem „Substanz(-ver)lust" auch rigoros vor die Füße gekotzt. Was D.O.S. hier vorführen, ist ein morbides und finstres … mehr. ...
We evaluated the role of VDR in the activation of the renin angiotensin system (RAS) in morphine-induced T cell loss. Morphine treated human T cells displayed down regulation of VDR and the activation of the RAS. On the other hand, a VDR agonist (EB1089) enhanced T cell VDR expression both under basal and morphine-stimulated states. Since T cells with silenced VDR displayed the activation of the RAS, whereas, activation of the VDR was associated with down regulation of the RAS, it appears that morphine-induced T cell RAS activation was dependent on the VDR status. Morphine also enhanced reactive oxygen species (ROS) generation in a dose dependent manner; however, this effect of morphine was inhibited by an opiate receptor antagonist, naltrexone. These findings confirmed the role of opiate receptors in morphine-induced ROS generation. Interestingly, the activation of VDR as well as blockade of Ang II (by losartan, an AT1 receptor blocker) also inhibited morphine-induced T cell ROS generation. ...
The local renin-angiotensin system (RAS) is closely related to bone metabolism. However, it is unknown whether the local RAS is related to bone mineral density (BMD) in glucocorticoid-induced osteoporosis (GIOP). Here, we revealed that the two main characteristics of GIOP might inhibit bone formation and enhance bone resorption. INTRODUCTION: The aim of this study is to assess the expression of the main RAS components in the trabecular bone of lumbar vertebrae in GIOP and analyze the relationship between the major RAS components and BMD. METHODS: We collected 96 inpatient cases of lumbar disc herniation from patients who underwent dual-energy X-ray absorptiometry examinations followed by surgical treatment in our hospital. Patients were divided into the GIOP group (n = 48) and control group (n = 48). The circulating and local expression levels of the main RAS components were examined. The correlation between the main RAS components and BMD was then analyzed. RESULTS: The mRNA expression of local ...
Blood-borne angiotensin II is generated from angiotensinogen via cleavage by renin and angiotensin-converting enzyme (ACE), an enzymatic cascade known as the renin-angiotensin system (RAS). Several lines of evidence indicate that ACE, beyond its classical role of mediating blood pressure regulation, might contribute to the etiology of substance addictions by influencing dopaminergic signaling. A functional insertion/deletion (I/D) polymorphism of the ACE gene was associated with risk for being a smoker among individuals with depression and with smoking severity in studies comprising patients with depression and healthy controls. Several reports have described significantly increased ACE activity in cerebrospinal fluid and serum among MS patients. Furthermore, in our previous work with MS patients from Croatian and Slovenian populations, we demonstrated that the ACE-I/D polymorphism contributes to an elevated MS risk among male patients. Here we investigated whether the ACE-I/D polymorphism might ...

Physiologic Investigation of the Renin Angiotensin Aldosterone Axis in HIV - Full Text View - ClinicalTrials.govPhysiologic Investigation of the Renin Angiotensin Aldosterone Axis in HIV - Full Text View - ClinicalTrials.gov

Angiotensinogen. Vasoconstrictor Agents. Serine Proteinase Inhibitors. Protease Inhibitors. Enzyme Inhibitors. Molecular ...
more infohttps://clinicaltrials.gov/show/NCT01407237?order=135

IJMS  | Free Full-Text | Angiotensin-Converting Enzymes Play a Dominant Role  in Fertility | HTMLIJMS | Free Full-Text | Angiotensin-Converting Enzymes Play a Dominant Role in Fertility | HTML

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): ...
more infohttp://mdpi.com/1422-0067/14/10/21071/htm

Vasoactive intestinal peptide down-regulates the intrahepatic renin-angiotensin system in the anaesthetized rat | Clinical...Vasoactive intestinal peptide down-regulates the intrahepatic renin-angiotensin system in the anaesthetized rat | Clinical...

VIP infusion decreased hepatic ACE activity (P , 0.05), the hepatic angiotensinogen concentration (P , 0.001) and the hepatic ... Angiotensin-converting enzyme (ACE) activity and angiotensinogen, angiotensin I, angiotensin II and renin concentrations were ... angiotensin I concentration (P , 0.05). The plasma angiotensinogen concentration and serum ACE activity were also decreased by ...
more infohttp://www.clinsci.org/content/99/3/201

RENIN ANGIOTENSIN ALDOSTERONE SYSTEM INHIBITORS					RENIN ANGIOTENSIN ALDOSTERONE SYSTEM INHIBITORS

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 ...
more infohttps://farmol.wordpress.com/2012/09/12/renin-angiotensin-aldosterone-system-inhibitors/

The lack of association between angiotensin-converting enzyme gene insertion/deletion polymorphism and nicotine dependence in...The lack of association between angiotensin-converting enzyme gene insertion/deletion polymorphism and nicotine dependence in...

Blood-borne angiotensin II is generated from angiotensinogen via cleavage by renin and angiotensin-converting enzyme (ACE), an ...
more infohttps://repository.medri.uniri.hr/en/islandora/object/medri%3A1447

Angiotensinogen | Define Angiotensinogen at Dictionary.comAngiotensinogen | Define Angiotensinogen at Dictionary.com

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 ...
more infohttp://www.dictionary.com/browse/angiotensinogen

Angiotensinogen DetectionAngiotensinogen Detection

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 ...
more infohttp://www.clontech.com/US/Products/Cell_Biology_and_Epigenetics/Metabolic_Diseases/Angiotensinogen?sitex=10020:22372:US&PEBCL1=JitTsn4IZGUahaPECvXdUw6u6R&PEBCL1_pses=ZG3359A5AD14C5BB509B474AE5A3AE58FADF4200D06DA0362B5A030E0C37F6D6085B643F38DBE88533A68BEC6A74FD59AC0C5AECDB761A60D5

Angiotensinogen Variants among Resistant Hypertensive PatientsAngiotensinogen Variants among Resistant Hypertensive Patients

... 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 ...
more infohttps://www.hindawi.com/journals/ijhy/2014/424793/

Molecular regulation of plasma and tissue angiotensinogen | SpringerLinkMolecular regulation of plasma and tissue angiotensinogen | SpringerLink

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 ...
more infohttps://link.springer.com/chapter/10.1007/978-94-009-0083-7_10

Angiotensinogen ELISA Kits | Biocompare.comAngiotensinogen ELISA Kits | Biocompare.com

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 ...
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Recombinant Human Angiotensinogen protein (ab191974)Recombinant Human Angiotensinogen protein (ab191974)

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). ...
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Gene transcriptions/Elements/Angiotensinogen core promoters - WikiversityGene transcriptions/Elements/Angiotensinogen core promoters - Wikiversity

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 ...
more infohttps://en.wikiversity.org/wiki/Angiotensinogen_core_promoter_element

Urinary angiotensinogen and risk of severe AKI.Urinary angiotensinogen and risk of severe AKI.

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. ...
more infohttp://www.biomedsearch.com/nih/Urinary-Angiotensinogen-Risk-Severe-AKI/23143504.html

Agt - Angiotensinogen precursor - Mus musculus (Mouse) - Agt gene & proteinAgt - Angiotensinogen precursor - Mus musculus (Mouse) - Agt gene & protein

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 ...
more infohttps://www.uniprot.org/uniprot/P11859

Agt - Angiotensinogen precursor - Rattus norvegicus (Rat) - Agt gene & proteinAgt - Angiotensinogen precursor - Rattus norvegicus (Rat) - Agt gene & protein

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 ...
more infohttps://www.uniprot.org/uniprot/P01015

WikiGenes - Agt - angiotensinogen (serpin peptidase...WikiGenes - Agt - angiotensinogen (serpin peptidase...

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 ...
more infohttps://www.wikigenes.org/e/gene/e/11606.html

Angiotensinogen Gene and Blood Pressure in the Japanese Population | HypertensionAngiotensinogen Gene and Blood Pressure in the Japanese Population | Hypertension

... 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 ...
more infohttp://hyper.ahajournals.org/content/25/4/688

Angiotensinogen Gene Knockout Delays and Attenuates Cold-Induced Hypertension | HypertensionAngiotensinogen Gene Knockout Delays and Attenuates Cold-Induced Hypertension | Hypertension

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 ...
more infohttp://hyper.ahajournals.org/content/41/2/322

Angiotensinogen Human ELISA | BioVendorAngiotensinogen Human ELISA | BioVendor

Angiotensinogen. By Technical Data. Angiotensinogen - Immunoassays. Angiotensinogen - Sandwich ELISA - Immunoassays. Human - ... Angiotensinogen - for Serum - Immunoassays. Angiotensinogen - for Urine - Immunoassays. Angiotensinogen - for Cerebrospinal ... Angiotensinogen - for Amniotic fluid - Immunoassays. Angiotensinogen - for Plasma - Immunoassays. Angiotensinogen - RUO - ... You are here: Home Products and Services Immunoassays Angiotensinogen Human ELISA Manufactured by BioVendor Angiotensinogen ...
more infohttps://www.biovendor.com/angiotensinogen-human-elisa

Renal Angiotensinogen Gene Expression and Tubular Atrophy in Diabetic Nephropathy | IntechOpenRenal Angiotensinogen Gene Expression and Tubular Atrophy in Diabetic Nephropathy | IntechOpen

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 ...
more infohttps://www.intechopen.com/books/diabetic-nephropathy/renal-angiotensinogen-gene-expression-and-tubular-atrophy-in-diabetic-nephropathy/

Prorenin, Renin, Angiotensinogen, and Angiotensin-Converting Enzyme in Normal and Failing Human Hearts | CirculationProrenin, Renin, Angiotensinogen, and Angiotensin-Converting Enzyme in Normal and Failing Human Hearts | Circulation

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 ...
more infohttp://circ.ahajournals.org/content/96/1/220

Human AGT / Angiotensinogen Quant ELISA Kit | Sandwich | LSBioHuman AGT / Angiotensinogen Quant ELISA Kit | Sandwich | LSBio

Angiotensinogen in Plasma, Serum. It is a Sandwich assay which can detect AGT / Angiotensinogen down to 15.6 pg/ml. ... Angiotensinogen ELISA Kit LS-F13066 is a 96-Well enzyme-linked immunosorbent assay for the Quantitative detection of Human AGT ... It is based upon a Sandwich assay principle and can be used to detect levels of AGT / Angiotensinogen as low as 15.6 picograms ... LS-F13066 is a 96-well enzyme-linked immunosorbent assay (ELISA) for the Quantitative detection of Human AGT / Angiotensinogen ...
more infohttps://www.lsbio.com/elisakits/human-agt-angiotensinogen-elisa-kit-sandwich-elisa-ls-f13066/13066

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. 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 ...
more infohttp://circ.ahajournals.org/content/early/2002/08/26/01.CIR.0000029093.93362.FC

Angiotensinogen elisa and antibodyAngiotensinogen elisa and antibody

Recombinant Protein and Angiotensinogen Antibody at MyBioSource. Custom ELISA Kit, Recombinant Protein and Antibody are ... Angiotensinogen. Angiotensinogen ELISA Kit. Angiotensinogen Recombinant. Angiotensinogen Antibody AGT ELISA Kit. AGT ... Angiotensinogen Essential component of the renin-angiotensin system (RAS), a potent regulator of blood pressure, body fluid and ... Also known as Angiotensinogen (Serpin A8).. Essential component of the renin-angiotensin system (RAS), a potent regulator of ...
more infohttps://www.mybiosource.com/proteins-family/angiotensinogen

The rapid purification and partial characterization of human serum angiotensinogen | Biochemical JournalThe rapid purification and partial characterization of human serum angiotensinogen | Biochemical Journal

The rapid purification and partial characterization of human serum angiotensinogen. C J Campbell, P A Charlton, C J Grinham, C ... The rapid purification and partial characterization of human serum angiotensinogen. C J Campbell, P A Charlton, C J Grinham, C ... Human angiotensinogen has been purified 390-fold from serum by a rapid high-yielding procedure that involved chromatography on ... The rapid purification and partial characterization of human serum angiotensinogen Message Subject (Your Name) has forwarded a ...
more infohttp://www.biochemj.org/content/243/1/121
  • Cardiac angiotensinogen was lower in DCM patients than in the donors, and its T/P ratio was half that for albumin, which is compatible with substrate consumption by cardiac renin. (ahajournals.org)
  • 10 11 12 13 Angiotensinogen mRNA is increased during postinfarction ventricular remodeling in the rat, 11 and ACE mRNA is increased during pressure overload-induced ventricular hypertrophy in the rat 12 and heart failure in humans. (ahajournals.org)
  • These affinity-purified antibodies recognize either mouse/rat or human angiotensinogen protein. (clontech.com)
  • The antibodies can be used for Western blot (WB) detection or immunohistochemical (IHC) detection of angiotensinogen protein. (clontech.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)
  • The M235T and T174M angiotensinogen mutations have been linked to increased risk for ischemic heart and cerebrovascular disease. (annals.org)
  • 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)
  • These data are the first to demonstrate the utility of angiotensinogen as a prognostic biomarker of AKI after cardiac surgery. (biomedsearch.com)
  • Angiotensinogen and ACE mRNAs have been detected in normal cardiac tissue. (ahajournals.org)
  • Angiotensinogen is an α-2-globulin produced constitutively and released into the circulation mainly by the liver. (wikiversity.org)
  • Angiotensinogen is mainly produced in the liver and secreted in plasma but also is synthesized in adipocytes, proximal tubule epithelial cells, and astrocytes. (biovendor.com)
  • Liver-derived angiotensinogen is cleaved in the circulating blood by renin to form Ang I, which is then converted by ACE, located on the luminal side of the vascular endothelium, into Ang II, a potent vasoconstrictor and stimulant of the release of aldosterone. (ahajournals.org)
  • It is based upon a Sandwich assay principle and can be used to detect levels of AGT / Angiotensinogen as low as 15.6 picograms per milliliter. (lsbio.com)
  • We hypothesized that adipocytes-derived angiotensinogen (Agt) played a critical role in adipogenesis and/or lipogenesis as well as adipose inflammation. (tennessee.edu)