An ANGIOTENSIN II analog which acts as a highly specific inhibitor of ANGIOTENSIN TYPE 1 RECEPTOR.
An amino acid intermediate in the metabolism of choline.
A FLAVOPROTEIN, this enzyme catalyzes the oxidation of SARCOSINE to GLYCINE; FORMALDEHYDE; and HYDROGEN PEROXIDE (H2O2).
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.
An essential branched-chain aliphatic amino acid found in many proteins. It is an isomer of LEUCINE. It is important in hemoglobin synthesis and regulation of blood sugar and energy levels.
A LIVER mitochondrial matrix flavoenzyme that catalyzes the oxidation of SARCOSINE to GLYCINE and FORMALDEHYDE. Mutation in the enzyme causes sarcosinemia, a rare autosomal metabolic defect characterized by elevated levels of SARCOSINE in BLOOD and URINE.
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.
Cell surface proteins that bind ANGIOTENSINS and trigger intracellular changes influencing the behavior of cells.
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.
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.
Agents that antagonize ANGIOTENSIN RECEPTORS. Many drugs in this class specifically target the ANGIOTENSIN TYPE 1 RECEPTOR.
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.
An antagonist of ANGIOTENSIN TYPE 1 RECEPTOR with antihypertensive activity due to the reduced pressor effect of ANGIOTENSIN II.
Tetrazoles are heterocyclic organic compounds containing a 1,3,5-triazole ring with an additional nitrogen atom, often used in pharmaceuticals as bioisosteres for carboxylic acid groups due to their isoelectronic nature and similar hydrogen bonding capabilities.
Agents that antagonize the ANGIOTENSIN II TYPE 2 RECEPTOR.
A heptapeptide formed from ANGIOTENSIN II after the removal of an amino acid at the N-terminal by AMINOPEPTIDASE A. Angiotensin III has the same efficacy as ANGIOTENSIN II in promoting ALDOSTERONE secretion and modifying renal blood flow, but less vasopressor activity (about 40%).
A FLAVOPROTEIN enzyme that catalyzes the oxidative demethylation of dimethylglycine to SARCOSINE and FORMALDEHYDE.
A family of sodium chloride-dependent neurotransmitter symporters that transport the amino acid GLYCINE. They differ from GLYCINE RECEPTORS, which signal cellular responses to GLYCINE. They are located primarily on the PLASMA MEMBRANE of NEURONS; GLIAL CELLS; EPITHELIAL CELLS; and RED BLOOD CELLS where they remove inhibitory neurotransmitter glycine from the EXTRACELLULAR SPACE.
An enzyme that catalyzes the METHYLATION of GLYCINE using S-ADENOSYLMETHIONINE to form SARCOSINE with the concomitant production of S-ADENOSYLHOMOCYSTEINE.
A branched-chain essential amino acid that has stimulant activity. It promotes muscle growth and tissue repair. It is a precursor in the penicillin biosynthetic pathway.
A class of drugs whose main indications are the treatment of hypertension and heart failure. They exert their hemodynamic effect mainly by inhibiting the renin-angiotensin system. They also modulate sympathetic nervous system activity and increase prostaglandin synthesis. They cause mainly vasodilation and mild natriuresis without affecting heart rate and contractility.
Biphenyl compounds are organic substances consisting of two phenyl rings connected by a single covalent bond, and can exhibit various properties and uses, including as intermediates in chemical synthesis, components in plastics and dyes, and as additives in fuels.
An octapeptide analog of angiotensin II (bovine) with amino acids 1 and 8 replaced with sarcosine and alanine, respectively. It is a highly specific competitive inhibitor of angiotensin II that is used in the diagnosis of HYPERTENSION.
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.
Compounds containing 1,3-diazole, a five membered aromatic ring containing two nitrogen atoms separated by one of the carbons. Chemically reduced ones include IMIDAZOLINES and IMIDAZOLIDINES. Distinguish from 1,2-diazole (PYRAZOLES).
Oxidoreductases, N-Demethylating are enzymes that catalyze the oxidation of N-methyl groups to carbonyl groups, typically found in xenobiotic metabolism, involving the removal of methyl groups from various substrates using molecular oxygen.
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.
Compounds with a BENZENE fused to IMIDAZOLES.
Drugs used to cause constriction of the blood vessels.
PRESSURE of the BLOOD on the ARTERIES and other BLOOD VESSELS.
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.
A non-essential amino acid. It is found primarily in gelatin and silk fibroin and used therapeutically as a nutrient. It is also a fast inhibitory neurotransmitter.
Drugs used in the treatment of acute or chronic vascular HYPERTENSION regardless of pharmacological mechanism. Among the antihypertensive agents are DIURETICS; (especially DIURETICS, THIAZIDE); ADRENERGIC BETA-ANTAGONISTS; ADRENERGIC ALPHA-ANTAGONISTS; ANGIOTENSIN-CONVERTING ENZYME INHIBITORS; CALCIUM CHANNEL BLOCKERS; GANGLIONIC BLOCKERS; and VASODILATOR AGENTS.
A hormone secreted by the ADRENAL CORTEX that regulates electrolyte and water balance by increasing the renal retention of sodium and the excretion of potassium.
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.
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.

Regulation of angiotensin II receptors and PKC isoforms by glucose in rat mesangial cells. (1/50)

It has been shown that glomerular angiotensin II (ANG II) receptors are downregulated and protein kinase C (PKC) is activated under diabetic conditions. We, therefore, investigated ANG II receptor and PKC isoform regulation in glomerular mesangial cells (MCs) under normal and elevated glucose concentrations. MCs were isolated from collagenase-treated rat glomeruli and cultured in medium containing normal or high glucose concentrations (5.5 and 25.0 mM, respectively). Competitive binding experiments were performed using the ANG II antagonists losartan and PD-123319, and PKC analysis was conducted by Western blotting. Competitive binding studies showed that the AT1 receptor was the only ANG II receptor detected on MCs grown to either subconfluence or confluence under either glucose concentration. AT1 receptor density was significantly downregulated in cells grown to confluence in high-glucose medium. Furthermore, elevated glucose concentration enhanced the presence of all MC PKC isoforms. In addition, PKCbeta, PKCgamma and PKCepsilon were translocated only in cells cultured in elevated glucose concentrations following 1-min stimulation by ANG II, whereas PKCalpha, PKCtheta, and PKClambda were translocated by ANG II only in cells grown in normal glucose. Moreover, no changes in the translocation of PKCdelta, PKCiota, PKCzeta, and PKCmu were detected in response to ANG II stimulation under euglycemic conditions. We conclude that MCs grown in high glucose concentration show altered ANG II receptor regulation as well as PKC isoform translocation compared with cells grown in normal glucose concentration.  (+info)

Cloning and characterization of ATRAP, a novel protein that interacts with the angiotensin II type 1 receptor. (2/50)

The carboxyl-terminal cytoplasmic domain of the angiotensin II type 1 (AT1) receptor has recently been shown to interact with several classes of cytoplasmic proteins that regulate different aspects of AT1 receptor physiology. Employing yeast two-hybrid screening of a mouse kidney cDNA library with the carboxyl-terminal cytoplasmic domain of the murine AT1a receptor as a bait, we have isolated a novel protein with a predicted molecular mass of 18 kDa, which we have named ATRAP (for AT1 receptor-associated protein). ATRAP interacts specifically with the carboxyl-terminal domain of the AT1a receptor but not with those of angiotensin II type 2 (AT2), m3 muscarinic acetylcholine, bradykinin B2, endothelin B, and beta2-adrenergic receptors. The mRNA of ATRAP was abundantly expressed in kidney, heart, and testis but was poorly expressed in lung, liver, spleen, and brain. The ATRAP-AT1a receptor association was confirmed by affinity chromatography, by specific co-immunoprecipitation of the two proteins, and by fluorescence microscopy, showing co-localization of these proteins in intact cells. Overexpression of ATRAP in COS-7 cells caused a marked inhibition of AT1a receptor-mediated activation of phospholipase C without affecting m3 receptor-mediated activation. In conclusion, we have isolated a novel protein that interacts specifically with the carboxyl-terminal cytoplasmic domain of the AT1a receptor and affects AT1a receptor signaling.  (+info)

Dynamic Ca2+ signalling in rat arterial smooth muscle cells under the control of local renin-angiotensin system. (3/50)

1. We visualized the changes in intracellular Ca2+ concentration ([Ca2+]i), using fluo-3 as an indicator, in individual smooth muscle cells within intact rat tail artery preparations. 2. On average in about 45 % of the vascular smooth muscle cells we found spontaneous Ca2+ waves and oscillations ( approximately 0.13 Hz), which we refer to here as Ca2+ ripples because the peak amplitude of [Ca2+]i was about one-seventh of that of Ca2+ oscillations evoked by noradrenaline. 3. We also found another pattern of spontaneous Ca2+ transients often in groups of two to three cells. They were rarely observed and are referred to as Ca2+ flashes because their peak amplitude was nearly twice as large as that in noradrenaline-evoked responses. 4. Sympathetic nerve activity was not considered responsible for the Ca2+ ripples, and they were abolished by inhibitors of either the Ca2+ pump in the sarcoplasmic reticulum (cyclopiazonic acid) or phospholipase C (U-73122). 5. Both angiotensin antagonists ([Sar1,Ile8]-angiotensin II and losartan) and an angiotensin converting enzyme inhibitor (captopril) inhibited the Ca2+ ripples. 6. The extracellular Ca2+-dependent tension borne by unstimulated arterial rings was reduced by the angiotensin antagonist by approximately 50 %. 7. These results indicate that the Ca2+ ripples are generated via inositol 1,4, 5-trisphosphate-induced Ca2+ release from the intracellular Ca2+ stores in response to locally produced angiotensin II, which contributes to the maintenance of vascular tone.  (+info)

Overexpression of angiotensin II type I receptor in cardiomyocytes induces cardiac hypertrophy and remodeling. (4/50)

Angiotensin II (AII) is a major determinant of arterial pressure and volume homeostasis, mainly because of its vascular action via the AII type 1 receptor (AT1R). AII has also been implicated in the development of cardiac hypertrophy because angiotensin I-converting enzyme inhibitors and AT1R antagonists prevent or regress ventricular hypertrophy in animal models and in human. However, because these treatments impede the action of AII at cardiac as well as vascular levels, and reduce blood pressure, it has been difficult to determine whether AII action on the heart is direct or a consequence of pressure-overload. To determine whether AII can induce cardiac hypertrophy directly via myocardial AT1R in the absence of vascular changes, transgenic mice overexpressing the human AT1R under the control of the mouse alpha-myosin heavy chain promoter were generated. Cardiomyocyte-specific overexpression of AT1R induced, in basal conditions, morphologic changes of myocytes and nonmyocytes that mimic those observed during the development of cardiac hypertrophy in human and in other mammals. These mice displayed significant cardiac hypertrophy and remodeling with increased expression of ventricular atrial natriuretic factor and interstitial collagen deposition and died prematurely of heart failure. Neither the systolic blood pressure nor the heart rate were changed. The data demonstrate a direct myocardial role for AII in the development of cardiac hypertrophy and failure and provide a useful model to elucidate the mechanisms of action of AII in the pathogenesis of cardiac diseases.  (+info)

Molecular cloning of a ferret angiotensin II AT(1) receptor reveals the importance of position 163 for Losartan binding. (5/50)

A complementary DNA for the angiotensin II (AngII) type 1 (AT(1)) receptor from Mustela putorius furo (ferret) was isolated from a ferret atria cDNA library. The cDNA encodes a protein (fAT(1)) of 359 amino acids having high homologies (93-99%) to other mammalian AT(1) receptor counterparts. When fAT(1) was expressed in COS-7 cells and photoaffinity labeled with the photoactive analogue (125)I- inverted question markSar(1), Bpa(8)AngII, a protein of 100 kDa was detected by autoradiography. The formation of this complex was specific since it was abolished in the presence of the AT(1) non-peptidic antagonist L-158,809. Functional analysis indicated that the fAT(1) receptor efficiently coupled to phospholipase C as demonstrated by an increase in inositol phosphate production following stimulation with AngII. Binding studies revealed that the fAT(1) receptor had a high affinity for the peptide antagonist inverted question markSar(1), Ile(8)AngII (K(d) of 5. 8+/-1.4 nM) but a low affinity for the AT(1) selective non-peptidic antagonist DuP 753 (K(d) of 91+/-15.6 nM). Interestingly, when we substituted Thr(163) with an Ala residue, which occupies this position in many mammalian AT(1) receptors, we restored the high affinity of this receptor for Dup 753 (11.7+/-5.13 nM). These results suggest that position 163 of the AT(1) receptor does not contribute to the overall binding of peptidic ligands but that certain non-peptidic antagonists such as Dup 753 are clearly dependent on this position for efficient binding.  (+info)

The luminal membrane of rat thick limb expresses AT1 receptor and aminopeptidase activities. (6/50)

BACKGROUND: Endogenous intratubular angiotensin II (Ang II) supports an autocrine tonic stimulation of NaCl absorption in the proximal tubule, and its production may be regulated independently of circulating Ang II. In addition, endogenous Ang II activity may be regulated at the brush border membrane (BBM), by the rate of aminopeptidase A and N (APA and APN) activities and the rate of Ca2+-independent phospholipase A2 (PLA2-dependent endocytosis and recycling of the complex Ang II subtype 1 (AT1) receptor (AT1-R). The aim of the present study was to look for subcellular localization of AT1-R, and APA and APN activities in the medullary thick ascending limb of Henle (mTAL), as well as search for an asymmetric coupling of AT1-R to signal transduction pathways. METHODS: Preparations of isolated basolateral membrane (BLMV) and luminal (LMV) membrane vesicles from rat mTAL were used to localize first, AT1-R by 125I-[Sar1, Ile8] Ang II binding studies and immunoblot experiments with a specific AT1-R antibody, and second, APA and APN activities. Microfluorometric monitoring of cytosolic Ca2+ with a Fura-2 probe was performed in mTAL microperfused in vitro, after apical or basolateral application of Ang II. RESULTS: AT1-R were present in both LMV and BLMV, with a similar Kd (nmol/L range) and Bmax. Accordingly, BLMV and LMV preparations similarly stained specific AT1-R antibody. APA and APN activities were selectively localized in LMV, although to a lesser extent than those measured in BBM. In the in vitro microperfused mTAL, basolateral but not apical Ang II induced a transient increase in cytosolic [Ca2+]. CONCLUSIONS: Besides the presence of basolateral AT1-R in mTAL coupled to the classical Ca2+-dependent transduction pathways, AT1-R are present in LMV, not coupled with Ca2+ signaling, and co-localized with APA and APN activities. Thus, apical APA and APN may play an important role in modulating endogenous Ang II activity on NaCl reabsorption in mTAL.  (+info)

AT1 receptors in the RVLM mediate pressor responses to emotional stress in rabbits. (7/50)

In this study, we examined the role of angiotensin type 1 (AT1) receptors in the rostral ventrolateral medulla (RVLM) in mediating the pressor action of emotional stress in conscious rabbits. Rabbits were chronically instrumented with guide cannulas for bilateral microinjections into the RVLM and an electrode for measuring renal sympathetic nerve activity (RSNA). Airjet stress evoked increases in arterial pressure, heart rate, and RSNA, which reached a maximum (+9+/-1 mm Hg, +20+/-5 beats/min, and +93+/-17%, respectively) in the first 2 minutes of stress exposure. Then RSNA rapidly returned to prestress values, while arterial pressure and heart rate remained close to the maximal level until the conclusion of the 7-minute airjet exposure. Microinjections of the nonselective angiotensin receptor antagonist sarile (0.5 nmol, n=8) or AT1 receptor antagonists losartan (2 nmol, n=6) or candesartan (0.2 nmol, n=6) into the RVLM did not alter resting cardiovascular parameters. By contrast, the antagonists attenuated the sustained phase (4 to 7 minutes) of the pressor stress response by 55% to 89%. However, only sarile decreased the onset of this response. The antagonists affected neither the stress-induced tachycardia nor the pressor response to glutamate microinjections. Microinfusion of angiotensin II (4 pmol/min, n=8) into the RVLM did not change the pressor response to airjet stress but attenuated tachycardic response by 47%. Microinjections of vehicle did not alter the cardiovascular stress response. Sarile, losartan, and angiotensin II did not affect the sympathoexcitatory response to baroreceptor unloading. These results suggest that AT1 receptors in the RVLM are important in mediating the pressor effects of emotional stress in conscious rabbits.  (+info)

Autocrine angiotensin system regulation of bovine aortic endothelial cell migration and plasminogen activator involves modulation of proto-oncogene pp60c-src expression. (8/50)

Rapid endothelial cell migration and inhibition of thrombosis are critical for the resolution of denudation injuries to the vessel wall. Inhibition of the endothelial cell autocrine angiotensin system, with either the angiotensin-converting enzyme inhibitor lisinopril or the angiotensin II receptor antagonist sar1, ile8-angiotensin II, leads to increased endothelial cell migration and urokinase-like plasminogen activator (u-PA) activity (Bell, L., and J. A. Madri. 1990. Am. J. Pathol. 137:7-12). Inhibition of the autocrine angiotensin system with the converting-enzyme inhibitor or the receptor antagonist also leads to increased expression of the proto-oncogene c-src: pp60c-src mRNA increased 7-11-fold, c-src protein 3-fold, and c-src kinase activity 2-3-fold. Endothelial cell expression of c-src was constitutively elevated after stable infection with a retroviral vector containing the c-src coding sequence. Constitutively increased c-src kinase activity reconstituted the increases in migration and u-PA observed with angiotensin system interruption. Antisera to bovine u-PA blocked the increase in migration associated with increased c-src expression. These data suggest that increases in endothelial cell migration and plasminogen activator after angiotensin system inhibition are at least partially pp60c-src mediated. Elevated c-src expression with angiotensin system inhibition may act to enhance intimal wound closure and to reduce luminal thrombogenicity in vivo.  (+info)

I am not aware of a specific medical definition for "1-Sarcosine-8-Isoleucine Angiotensin II." It is possible that this term is being used to describe an altered or modified form of the peptide hormone angiotensin II.

Angiotensin II is a powerful vasoconstrictor and plays a central role in the regulation of blood pressure and fluid balance. Its octapeptide structure consists of eight amino acids, with the sequence Asp-Arg-Val-Tyr-Ile-His-Pro-Phe.

Modifying this sequence by replacing one or more amino acids can result in altered biological activity. In this case, "1-Sarcosine-8-Isoleucine" suggests that the first amino acid (Aspartic Acid) has been replaced with Sarcosine (N-methylglycine), and the eighth amino acid (Phenylalanine) has been replaced with Isoleucine.

However, without further context or research, it is difficult to provide a precise medical definition for this term. If you are seeking information on a specific scientific study or application, please provide more details so that I can give a more informed response.

Sarcosine is not a medical condition or disease, but rather it is an organic compound that is classified as a natural amino acid. It is a metabolite that can be found in the human body, and it is involved in various biochemical processes. Specifically, sarcosine is formed from the conversion of the amino acid glycine by the enzyme glycine sarcosine N-methyltransferase (GSMT) and is then converted to glycine betaine (also known as trimethylglycine) by the enzyme betaine-homocysteine S-methyltransferase (BHMT).

Abnormal levels of sarcosine have been found in various disease states, including cancer. Some studies have suggested that high levels of sarcosine in urine or prostate tissue may be associated with an increased risk of developing prostate cancer or a more aggressive form of the disease. However, more research is needed to confirm these findings and establish the clinical significance of sarcosine as a biomarker for cancer or other diseases.

Sarcosine oxidase is an enzyme that plays a role in the metabolism of certain amino acids. Specifically, it catalyzes the oxidation of sarcosine (also known as N-methylglycine) to form glycine, formaldehyde, and hydrogen peroxide. This reaction is an important step in the catabolism of certain amino acids, such as glycine, sarcosine, and betaine, and helps to generate energy for the cell.

Sarcosine oxidase is a complex enzyme that consists of two subunits: a catalytic subunit that contains the active site where the chemical reaction takes place, and a regulatory subunit that helps to control the activity of the enzyme. The enzyme requires several cofactors, including molybdenum, iron, and flavin adenine dinucleotide (FAD), in order to function properly.

Deficiencies or mutations in sarcosine oxidase can lead to various metabolic disorders, such as glycine encephalopathy (also known as non-ketotic hyperglycinemia), which is characterized by an accumulation of glycine in the body and can cause neurological symptoms.

Angiotensin II is a potent vasoactive peptide hormone that plays a critical role in the renin-angiotensin-aldosterone system (RAAS), which is a crucial regulator of blood pressure and fluid balance in the body. It is formed from angiotensin I through the action of an enzyme called angiotensin-converting enzyme (ACE).

Angiotensin II has several physiological effects on various organs, including:

1. Vasoconstriction: Angiotensin II causes contraction of vascular smooth muscle, leading to an increase in peripheral vascular resistance and blood pressure.
2. Aldosterone release: Angiotensin II stimulates the adrenal glands to release aldosterone, a hormone that promotes sodium reabsorption and potassium excretion in the kidneys, thereby increasing water retention and blood volume.
3. Sympathetic nervous system activation: Angiotensin II activates the sympathetic nervous system, leading to increased heart rate and contractility, further contributing to an increase in blood pressure.
4. Thirst regulation: Angiotensin II stimulates the hypothalamus to increase thirst, promoting water intake and helping to maintain intravascular volume.
5. Cell growth and fibrosis: Angiotensin II has been implicated in various pathological processes, such as cell growth, proliferation, and fibrosis, which can contribute to the development of cardiovascular and renal diseases.

Angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) are two classes of medications commonly used in clinical practice to target the RAAS by blocking the formation or action of angiotensin II, respectively. These drugs have been shown to be effective in managing hypertension, heart failure, and chronic kidney disease.

Isoleucine is an essential branched-chain amino acid, meaning it cannot be synthesized by the human body and must be obtained through dietary sources. Its chemical formula is C6H13NO2. Isoleucine is crucial for muscle protein synthesis, hemoglobin formation, and energy regulation during exercise or fasting. It is found in various foods such as meat, fish, eggs, dairy products, legumes, and nuts. Deficiency of isoleucine may lead to various health issues like muscle wasting, fatigue, and mental confusion.

Sarcosine Dehydrogenase (SDH) is an mitochondrial enzyme complex that plays a crucial role in the metabolism of certain amino acids. Specifically, SDH catalyzes the oxidation of sarcosine (N-methylglycine) to glycine, generating NAD+ from NADH in the process. This enzyme complex is composed of four subunits (SDHA, SDHB, SDHC, and SDHD), all of which are encoded by nuclear genes.

Deficiencies or mutations in any of the SDH subunits can lead to a variety of clinical manifestations, including neurological disorders, tumorigenesis, and mitochondrial diseases. For instance, mutations in SDHA, SDHB, SDHC, and SDHD have been associated with hereditary paragangliomas and pheochromocytomas, which are rare neuroendocrine tumors that arise from the chromaffin cells of the sympathetic nervous system.

SDH is also part of the tricarboxylic acid (TCA) cycle, also known as the Krebs cycle or citric acid cycle, which is a central metabolic pathway involved in energy production and biosynthesis. Therefore, SDH deficiencies can have profound effects on cellular metabolism and homeostasis, leading to various pathological conditions.

The Angiotensin II Receptor Type 1 (AT1 receptor) is a type of G protein-coupled receptor that binds and responds to the hormone angiotensin II, which plays a crucial role in the renin-angiotensin-aldosterone system (RAAS). The RAAS is a vital physiological mechanism that regulates blood pressure, fluid, and electrolyte balance.

The AT1 receptor is found in various tissues throughout the body, including the vascular smooth muscle cells, cardiac myocytes, adrenal glands, kidneys, and brain. When angiotensin II binds to the AT1 receptor, it activates a series of intracellular signaling pathways that lead to vasoconstriction, increased sodium and water reabsorption in the kidneys, and stimulation of aldosterone release from the adrenal glands. These effects ultimately result in an increase in blood pressure and fluid volume.

AT1 receptor antagonists, also known as angiotensin II receptor blockers (ARBs), are a class of drugs used to treat hypertension, heart failure, and other cardiovascular conditions. By blocking the AT1 receptor, these medications prevent angiotensin II from exerting its effects on the cardiovascular system, leading to vasodilation, decreased sodium and water reabsorption in the kidneys, and reduced aldosterone release. These actions ultimately result in a decrease in blood pressure and fluid volume.

Angiotensin receptors are a type of G protein-coupled receptor that binds the angiotensin peptides, which are important components of the renin-angiotensin-aldosterone system (RAAS). The RAAS is a hormonal system that regulates blood pressure and fluid balance.

There are two main types of angiotensin receptors: AT1 and AT2. Activation of AT1 receptors leads to vasoconstriction, increased sodium and water reabsorption in the kidneys, and cell growth and proliferation. On the other hand, activation of AT2 receptors has opposite effects, such as vasodilation, natriuresis (increased excretion of sodium in urine), and anti-proliferative actions.

Angiotensin II is a potent activator of AT1 receptors, while angiotensin IV has high affinity for AT2 receptors. Angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) are two classes of drugs that target the RAAS by blocking the formation or action of angiotensin II, leading to decreased activation of AT1 receptors and improved cardiovascular outcomes.

Angiotensin II Type 1 Receptor Blockers (ARBs) are a class of medications used to treat hypertension, heart failure, and protect against kidney damage in patients with diabetes. They work by blocking the action of angiotensin II, a hormone that causes blood vessels to constrict and blood pressure to increase, at its type 1 receptor. By blocking this effect, ARBs cause blood vessels to dilate, reducing blood pressure and decreasing the workload on the heart. Examples of ARBs include losartan, valsartan, irbesartan, and candesartan.

The Angiotensin II Receptor Type 2 (AT2R) is a type of G protein-coupled receptor that binds to the hormone angiotensin II, which plays a crucial role in the renin-angiotensin system (RAS), a vital component in regulating blood pressure and fluid balance.

The AT2R is expressed in various tissues, including the heart, blood vessels, kidneys, brain, and reproductive organs. When angiotensin II binds to the AT2R, it initiates several signaling pathways that can lead to vasodilation, anti-proliferation, anti-inflammation, and neuroprotection.

In contrast to the Angiotensin II Receptor Type 1 (AT1R), which is primarily associated with vasoconstriction, sodium retention, and fibrosis, AT2R activation has been shown to have protective effects in several pathological conditions, including hypertension, heart failure, atherosclerosis, and kidney disease.

However, the precise functions of AT2R are still being investigated, and its role in various physiological and pathophysiological processes may vary depending on the tissue type and context.

Angiotensin receptor antagonists (ARAs), also known as angiotensin II receptor blockers (ARBs), are a class of medications used to treat hypertension, heart failure, and protect against kidney damage in patients with diabetes. They work by blocking the action of angiotensin II, a potent vasoconstrictor and hormone that increases blood pressure and promotes tissue fibrosis. By blocking the binding of angiotensin II to its receptors, ARAs cause relaxation of blood vessels, decreased sodium and water retention, and reduced cardiac remodeling, ultimately leading to improved cardiovascular function and reduced risk of organ damage. Examples of ARAs include losartan, valsartan, irbesartan, and candesartan.

Angiotensin I is a decapeptide (a peptide consisting of ten amino acids) that is generated by the action of an enzyme called renin on a protein called angiotensinogen. Renin cleaves angiotensinogen to produce angiotensin I, which is then converted to angiotensin II by the action of an enzyme called angiotensin-converting enzyme (ACE).

Angiotensin II is a potent vasoconstrictor, meaning it causes blood vessels to narrow and blood pressure to increase. It also stimulates the release of aldosterone from the adrenal glands, which leads to increased sodium and water reabsorption in the kidneys, further increasing blood volume and blood pressure.

Angiotensin I itself has little biological activity, but it is an important precursor to angiotensin II, which plays a key role in regulating blood pressure and fluid balance in the body.

Losartan is an angiotensin II receptor blocker (ARB) medication that is primarily used to treat hypertension (high blood pressure), but can also be used to manage chronic heart failure and protect against kidney damage in patients with type 2 diabetes. It works by blocking the action of angiotensin II, a hormone that causes blood vessels to narrow and blood pressure to rise. By blocking this hormone's effects, losartan helps relax and widen blood vessels, making it easier for the heart to pump blood and reducing the workload on the cardiovascular system.

The medical definition of losartan is: "A synthetic angiotensin II receptor antagonist used in the treatment of hypertension, chronic heart failure, and diabetic nephropathy. It selectively blocks the binding of angiotensin II to the AT1 receptor, leading to vasodilation, decreased aldosterone secretion, and increased renin activity."

Tetrazoles are a class of heterocyclic aromatic organic compounds that contain a five-membered ring with four nitrogen atoms and one carbon atom. They have the chemical formula of C2H2N4. Tetrazoles are stable under normal conditions, but can decompose explosively when heated or subjected to strong shock.

In the context of medicinal chemistry, tetrazoles are sometimes used as bioisosteres for carboxylic acids, as they can mimic some of their chemical and biological properties. This has led to the development of several drugs that contain tetrazole rings, such as the antiviral drug tenofovir and the anti-inflammatory drug celecoxib.

However, it's important to note that 'tetrazoles' is not a medical term per se, but rather a chemical term that can be used in the context of medicinal chemistry or pharmacology.

Angiotensin II Type 2 Receptor Blockers (AT2RBs) are a class of drugs that selectively block the activation of Angiotensin II Type 2 receptors (AT2R). These receptors are found in various tissues throughout the body and play a role in regulating blood pressure, inflammation, and cell growth.

Angiotensin II is a hormone that constricts blood vessels and increases blood pressure. It binds to both AT1R and AT2R, but its effects are mainly mediated through AT1R. AT2RBs work by blocking the action of Angiotensin II at the AT2R, which can help lower blood pressure and reduce inflammation.

AT2RBs have been shown to have potential benefits in various clinical settings, including heart failure, diabetes, and kidney disease. However, their use is not as widespread as angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs), which primarily target the AT1R.

Some examples of AT2RBs include EMA401, PD123319, and TRV120027.

Angiotensin III is a hormone that is involved in the regulation of blood pressure and fluid balance in the body. It is formed by the enzymatic breakdown of angiotensin II, another hormone in the renin-angiotensin system (RAS). Angiotensin III has similar physiological effects as angiotensin II, including vasoconstriction (narrowing of blood vessels), stimulation of aldosterone release from the adrenal glands (which leads to sodium and water retention), and stimulation of thirst.

Angiotensin III is a peptide consisting of three amino acids, namely arginine-valine-tyrosine (Arg-Val-Tyr). It binds to and activates the angiotensin II receptor type 1 (AT1) and type 2 (AT2), which are found in various tissues throughout the body. The activation of these receptors leads to a range of physiological responses, including increased blood pressure, heart rate, and fluid volume.

Angiotensin III is less potent than angiotensin II in its ability to cause vasoconstriction and aldosterone release, but it has been shown to have important roles in the regulation of cardiovascular function, particularly during conditions of reduced renal perfusion or low blood pressure. It may also contribute to the development of certain diseases, such as hypertension, heart failure, and kidney disease.

Dimethylglycine dehydrogenase is an enzyme that plays a role in the metabolism of certain amino acids. The systematic name for this enzyme is N,N-dimethylglycine:electron transfer flavoprotein oxidoreductase. It catalyzes the following chemical reaction:

N,N-dimethylglycine + electron transfer flavoprotein → sarcosine + formaldehyde + reduced electron transfer flavoprotein

This enzyme is found in many organisms, including bacteria and humans. In humans, it is located in the mitochondria and is involved in the breakdown of the amino acid glycine. Mutations in the gene that encodes this enzyme can lead to a rare genetic disorder called dimethylglycine dehydrogenase deficiency, which is characterized by developmental delay, intellectual disability, and seizures.

Glycine is an important amino acid that plays a role in various physiological processes in the human body. Plasma membrane transport proteins are specialized molecules found in the cell membrane that facilitate the movement of specific molecules, such as ions or neurotransmitters like glycine, into and out of cells.

Glycine plasma membrane transport proteins specifically regulate the transcellular movement of glycine across the plasma membrane. These transport proteins belong to a family of solute carriers (SLC) known as the glycine transporters (GlyTs). There are two main isoforms, GlyT1 and GlyT2, which differ in their distribution, function, and regulation.

GlyT1 is widely expressed throughout the central nervous system and plays a crucial role in terminating glycinergic neurotransmission by rapidly removing glycine from the synaptic cleft. This isoform is also involved in regulating extracellular glycine concentrations in various tissues, including the brainstem, spinal cord, and retina.

GlyT2, on the other hand, is primarily localized to presynaptic terminals of glycinergic neurons, where it functions as a vesicular glycine transporter (VGT). Its primary role is to transport glycine into synaptic vesicles for subsequent release into the synapse during neurotransmission.

Dysfunction in glycine plasma membrane transport proteins has been implicated in several neurological disorders, such as hyperekplexia (startle disease) and certain forms of epilepsy. In these cases, impaired glycinergic neurotransmission can lead to motor and cognitive deficits, highlighting the importance of proper glycine transport protein function for normal physiological processes.

Glycine N-Methyltransferase (GNMT) is an enzyme that plays a crucial role in methionine and homocysteine metabolism. It is primarily found in the liver and to some extent in the kidneys, pancreas, and brain.

GNMT catalyzes the transfer of a methyl group from S-adenosylmethionine (SAM) to glycine, forming S-adenosylhomocysteine (SAH) and sarcosine as products. This reaction helps regulate the levels of SAM, SAH, and homocysteine in the body.

Additionally, GNMT has been shown to have other functions, such as detoxification of xenobiotics and regulation of lipid metabolism. Abnormal GNMT activity or expression has been linked to various diseases, including liver disorders, cardiovascular disease, and cancer.

Valine is an essential amino acid, meaning it cannot be produced by the human body and must be obtained through diet. It is a hydrophobic amino acid, with a branched side chain, and is necessary for the growth, repair, and maintenance of tissues in the body. Valine is also important for muscle metabolism, and is often used by athletes as a supplement to enhance physical performance. Like other essential amino acids, valine must be obtained through foods such as meat, fish, dairy products, and legumes.

Angiotensin-Converting Enzyme (ACE) inhibitors are a class of medications that are commonly used to treat various cardiovascular conditions, such as hypertension (high blood pressure), heart failure, and diabetic nephropathy (kidney damage in people with diabetes).

ACE inhibitors work by blocking the action of angiotensin-converting enzyme, an enzyme that converts the hormone angiotensin I to angiotensin II. Angiotensin II is a potent vasoconstrictor, meaning it narrows blood vessels and increases blood pressure. By inhibiting the conversion of angiotensin I to angiotensin II, ACE inhibitors cause blood vessels to relax and widen, which lowers blood pressure and reduces the workload on the heart.

Some examples of ACE inhibitors include captopril, enalapril, lisinopril, ramipril, and fosinopril. These medications are generally well-tolerated, but they can cause side effects such as cough, dizziness, headache, and elevated potassium levels in the blood. It is important for patients to follow their healthcare provider's instructions carefully when taking ACE inhibitors and to report any unusual symptoms or side effects promptly.

Biphenyl compounds, also known as diphenyls, are a class of organic compounds consisting of two benzene rings linked by a single carbon-carbon bond. The chemical structure of biphenyl compounds can be represented as C6H5-C6H5. These compounds are widely used in the industrial sector, including as intermediates in the synthesis of other chemicals, as solvents, and in the production of plastics and dyes. Some biphenyl compounds also have biological activity and can be found in natural products. For example, some plant-derived compounds that belong to this class have been shown to have anti-inflammatory, antioxidant, and anticancer properties.

Saralasin is a synthetic analog of the natural hormone angiotensin II, which is used in research and medicine. It acts as an antagonist of the angiotensin II receptor, blocking its effects. Saralasin is primarily used in research to study the role of the renin-angiotensin system in various physiological processes. In clinical medicine, it has been used in the diagnosis and treatment of conditions such as hypertension and pheochromocytoma, although its use is not widespread due to the availability of more effective and selective drugs.

Peptidyl-dipeptidase A is more commonly known as angiotensin-converting enzyme (ACE). It is a key enzyme in the renin-angiotensin-aldosterone system (RAAS), which regulates blood pressure and fluid balance.

ACE is a membrane-bound enzyme found primarily in the lungs, but also in other tissues such as the heart, kidneys, and blood vessels. It plays a crucial role in converting the inactive decapeptide angiotensin I into the potent vasoconstrictor octapeptide angiotensin II, which constricts blood vessels and increases blood pressure.

ACE also degrades the peptide bradykinin, which is involved in the regulation of blood flow and vascular permeability. By breaking down bradykinin, ACE helps to counteract its vasodilatory effects, thereby maintaining blood pressure homeostasis.

Inhibitors of ACE are widely used as medications for the treatment of hypertension, heart failure, and diabetic kidney disease, among other conditions. These drugs work by blocking the action of ACE, leading to decreased levels of angiotensin II and increased levels of bradykinin, which results in vasodilation, reduced blood pressure, and improved cardiovascular function.

Imidazoles are a class of heterocyclic organic compounds that contain a double-bonded nitrogen atom and two additional nitrogen atoms in the ring. They have the chemical formula C3H4N2. In a medical context, imidazoles are commonly used as antifungal agents. Some examples of imidazole-derived antifungals include clotrimazole, miconazole, and ketoconazole. These medications work by inhibiting the synthesis of ergosterol, a key component of fungal cell membranes, leading to increased permeability and death of the fungal cells. Imidazoles may also have anti-inflammatory, antibacterial, and anticancer properties.

Oxidoreductases are a class of enzymes that catalyze oxidation-reduction reactions, where a electron is transferred from one molecule to another. N-Demethylating oxidoreductases are a specific subclass of these enzymes that catalyze the removal of a methyl group (-CH3) from a nitrogen atom (-N) in a molecule, which is typically a xenobiotic compound (a foreign chemical substance found within an living organism). This process often involves the transfer of electrons and the formation of water as a byproduct.

The reaction catalyzed by N-demethylating oxidoreductases can be represented as follows:
R-N-CH3 + O2 + H2O → R-N-H + CH3OH + H2O2

where R represents the rest of the molecule. The removal of the methyl group is often an important step in the metabolism and detoxification of xenobiotic compounds, as it can make them more water soluble and facilitate their excretion from the body.

Renin is a medically recognized term and it is defined as:

"A protein (enzyme) that is produced and released by specialized cells (juxtaglomerular cells) in the kidney. Renin is a key component of the renin-angiotensin-aldosterone system (RAAS), which helps regulate blood pressure and fluid balance in the body.

When the kidney detects a decrease in blood pressure or a reduction in sodium levels, it releases renin into the bloodstream. Renin then acts on a protein called angiotensinogen, converting it to angiotensin I. Angiotensin-converting enzyme (ACE) subsequently converts angiotensin I to angiotensin II, which is a potent vasoconstrictor that narrows blood vessels and increases blood pressure.

Additionally, angiotensin II stimulates the adrenal glands to release aldosterone, a hormone that promotes sodium reabsorption in the kidneys and increases water retention, further raising blood pressure.

Therefore, renin plays a critical role in maintaining proper blood pressure and electrolyte balance in the body."

Benzimidazoles are a class of heterocyclic compounds containing a benzene fused to a imidazole ring. They have a wide range of pharmacological activities and are used in the treatment of various diseases. Some of the benzimidazoles are used as antiparasitics, such as albendazole and mebendazole, which are effective against a variety of worm infestations. Other benzimidazoles have antifungal properties, such as thiabendazole and fuberidazole, and are used to treat fungal infections. Additionally, some benzimidazoles have been found to have anti-cancer properties and are being investigated for their potential use in cancer therapy.

Vasoconstrictor agents are substances that cause the narrowing of blood vessels by constricting the smooth muscle in their walls. This leads to an increase in blood pressure and a decrease in blood flow. They work by activating the sympathetic nervous system, which triggers the release of neurotransmitters such as norepinephrine and epinephrine that bind to alpha-adrenergic receptors on the smooth muscle cells of the blood vessel walls, causing them to contract.

Vasoconstrictor agents are used medically for a variety of purposes, including:

* Treating hypotension (low blood pressure)
* Controlling bleeding during surgery or childbirth
* Relieving symptoms of nasal congestion in conditions such as the common cold or allergies

Examples of vasoconstrictor agents include phenylephrine, oxymetazoline, and epinephrine. It's important to note that prolonged use or excessive doses of vasoconstrictor agents can lead to rebound congestion and other adverse effects, so they should be used with caution and under the guidance of a healthcare professional.

Blood pressure is the force exerted by circulating blood on the walls of the blood vessels. It is measured in millimeters of mercury (mmHg) and is given as two figures:

1. Systolic pressure: This is the pressure when the heart pushes blood out into the arteries.
2. Diastolic pressure: This is the pressure when the heart rests between beats, allowing it to fill with blood.

Normal blood pressure for adults is typically around 120/80 mmHg, although this can vary slightly depending on age, sex, and other factors. High blood pressure (hypertension) is generally considered to be a reading of 130/80 mmHg or higher, while low blood pressure (hypotension) is usually defined as a reading below 90/60 mmHg. It's important to note that blood pressure can fluctuate throughout the day and may be affected by factors such as stress, physical activity, and medication use.

Angiotensins are a group of hormones that play a crucial role in the body's cardiovascular system, particularly in regulating blood pressure and fluid balance. The most well-known angiotensins are Angiotensin I, Angiotensin II, and Angiotensin-(1-7).

Angiotensinogen is a protein produced mainly by the liver. When the body requires an increase in blood pressure, renin (an enzyme produced by the kidneys) cleaves angiotensinogen to form Angiotensin I. Then, another enzyme called angiotensin-converting enzyme (ACE), primarily found in the lungs, converts Angiotensin I into Angiotensin II.

Angiotensin II is a potent vasoconstrictor, causing blood vessels to narrow and increase blood pressure. It also stimulates the release of aldosterone from the adrenal glands, which leads to increased sodium reabsorption in the kidneys, further raising blood pressure and promoting fluid retention.

Angiotensin-(1-7) is a more recently discovered member of the angiotensin family. It has opposing effects to Angiotensin II, acting as a vasodilator and counterbalancing some of the negative consequences of Angiotensin II's actions.

Medications called ACE inhibitors and ARBs (angiotensin receptor blockers) are commonly used in clinical practice to target the renin-angiotensin system, lowering blood pressure and protecting against organ damage in various cardiovascular conditions.

Glycine is a simple amino acid that plays a crucial role in the body. According to the medical definition, glycine is an essential component for the synthesis of proteins, peptides, and other biologically important compounds. It is also involved in various metabolic processes, such as the production of creatine, which supports muscle function, and the regulation of neurotransmitters, affecting nerve impulse transmission and brain function. Glycine can be found as a free form in the body and is also present in many dietary proteins.

Antihypertensive agents are a class of medications used to treat high blood pressure (hypertension). They work by reducing the force and rate of heart contractions, dilating blood vessels, or altering neurohormonal activation to lower blood pressure. Examples include diuretics, beta blockers, ACE inhibitors, ARBs, calcium channel blockers, and direct vasodilators. These medications may be used alone or in combination to achieve optimal blood pressure control.

Aldosterone is a hormone produced by the adrenal gland. It plays a key role in regulating sodium and potassium balance and maintaining blood pressure through its effects on the kidneys. Aldosterone promotes the reabsorption of sodium ions and the excretion of potassium ions in the distal tubules and collecting ducts of the nephrons in the kidneys. This increases the osmotic pressure in the blood, which in turn leads to water retention and an increase in blood volume and blood pressure.

Aldosterone is released from the adrenal gland in response to a variety of stimuli, including angiotensin II (a peptide hormone produced as part of the renin-angiotensin-aldosterone system), potassium ions, and adrenocorticotropic hormone (ACTH) from the pituitary gland. The production of aldosterone is regulated by a negative feedback mechanism involving sodium levels in the blood. High sodium levels inhibit the release of aldosterone, while low sodium levels stimulate its release.

In addition to its role in maintaining fluid and electrolyte balance and blood pressure, aldosterone has been implicated in various pathological conditions, including hypertension, heart failure, and primary hyperaldosteronism (a condition characterized by excessive production of aldosterone).

Hypertension is a medical term used to describe abnormally high blood pressure in the arteries, often defined as consistently having systolic blood pressure (the top number in a blood pressure reading) over 130 mmHg and/or diastolic blood pressure (the bottom number) over 80 mmHg. It is also commonly referred to as high blood pressure.

Hypertension can be classified into two types: primary or essential hypertension, which has no identifiable cause and accounts for about 95% of cases, and secondary hypertension, which is caused by underlying medical conditions such as kidney disease, hormonal disorders, or use of certain medications.

If left untreated, hypertension can lead to serious health complications such as heart attack, stroke, heart failure, and chronic kidney disease. Therefore, it is important for individuals with hypertension to manage their condition through lifestyle modifications (such as healthy diet, regular exercise, stress management) and medication if necessary, under the guidance of a healthcare professional.

Sprague-Dawley rats are a strain of albino laboratory rats that are widely used in scientific research. They were first developed by researchers H.H. Sprague and R.C. Dawley in the early 20th century, and have since become one of the most commonly used rat strains in biomedical research due to their relatively large size, ease of handling, and consistent genetic background.

Sprague-Dawley rats are outbred, which means that they are genetically diverse and do not suffer from the same limitations as inbred strains, which can have reduced fertility and increased susceptibility to certain diseases. They are also characterized by their docile nature and low levels of aggression, making them easier to handle and study than some other rat strains.

These rats are used in a wide variety of research areas, including toxicology, pharmacology, nutrition, cancer, and behavioral studies. Because they are genetically diverse, Sprague-Dawley rats can be used to model a range of human diseases and conditions, making them an important tool in the development of new drugs and therapies.

Ip S, Tsang S, Wong T, Che C, Leung P (2003). "Saralasin, a nonspecific angiotensin II receptor antagonist, attenuates ... isoleucine is replaced by valine, and at position 8, phenylalanine is replaced by alanine which leads to a smaller stimulatory ... sarcosine replaces aspartic acid increasing the affinity for vascular smooth muscle receptors and making the peptide resistant ... Saralasin is a competitive angiotensin II receptor antagonist with partial agonist activity. The aminopeptide sequence for ...
... angiotensin i MeSH D23.469.050.050.050 - angiotensin ii MeSH D23.469.050.050.050.050 - angiotensin amide MeSH D23.469.050.050. ... type ii MeSH D23.101.100.110.925 - e-selectin MeSH D23.101.100.110.930 - p-selectin MeSH D23.101.100.110.970 - vascular cell ... type ii MeSH D23.050.301.264.035.915 - p-selectin MeSH D23.050.301.264.035.920 - vascular cell adhesion molecule-1 MeSH D23.050 ... histocompatibility antigens class ii MeSH D23.050.301.500.410.400 - hla-d antigens MeSH D23.050.301.500.410.400.420 - HLA-DP ...
... angiotensin i MeSH D12.644.456.073.041 - angiotensin ii MeSH D12.644.456.073.041.050 - angiotensin amide MeSH D12.644.456.073. ... angiotensin i MeSH D12.644.400.070.078 - angiotensin ii MeSH D12.644.400.070.080 - angiotensin iii MeSH D12.644.400.085 - ... casein kinase ii MeSH D12.644.360.200 - cyclic nucleotide-regulated protein kinases MeSH D12.644.360.200.125 - cyclic amp- ... interferon type ii MeSH D12.644.276.174.440.893.510 - interferon-gamma, recombinant MeSH D12.644.276.174.480 - lymphokines MeSH ...
... type II: EC 5.99.1.3) 6-carboxytetrahydropterin synthase Category:EC 6.1.1 FARSB (EC 6.1.1.20) EC 6.2.1.1: Acetate-CoA ligase ... L-allo-isoleucine--holo-CmaA peptidyl-carrier protein ligase EC 6.2.1.47: Medium-chain-fatty-acid-(acyl-carrier-protein) ligase ... EC 3.4.15 Angiotensin converting enzyme Category:EC 3.4.21 Serine protease Chymotrypsin (EC 3.4.21.1) Trypsin (EC 3.4.21.4) ... Sarcosine oxidase EC 1.5.3.1 Dihydrobenzophenanthridine oxidase EC 1.5.3.12 Category:EC 1.5.4 (with a disulfide as acceptor) ...
Ip S, Tsang S, Wong T, Che C, Leung P (2003). "Saralasin, a nonspecific angiotensin II receptor antagonist, attenuates ... isoleucine is replaced by valine, and at position 8, phenylalanine is replaced by alanine which leads to a smaller stimulatory ... sarcosine replaces aspartic acid increasing the affinity for vascular smooth muscle receptors and making the peptide resistant ... Saralasin is a competitive angiotensin II receptor antagonist with partial agonist activity. The aminopeptide sequence for ...
3-methylglutaconicaciduria type II use Barth Syndrome 3-Methylindole use Skatole 3-O-Methyl-D-Glucose use 3-O-Methylglucose ... 7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide 7,8-Dihydroxy-9,10-Epoxy-7,8,9,10-Tetrahydrobenzo(a)pyrene use 7,8-Dihydro-7 ... 2-Amino-5-phosphonovaleric Acid use 2-Amino-5-phosphonovalerate 2-Amino-6-(1,2,3-trihydroxypropyl)-4(3H)-pteridinone use ... 2-Dehydro-3-Deoxyphosphoheptonate Aldolase use 3-Deoxy-7-Phosphoheptulonate Synthase 2-Fluoro-2-deoxy-D-glucose use ...
3-methylglutaconicaciduria type II use Barth Syndrome 3-Methylindole use Skatole 3-O-Methyl-D-Glucose use 3-O-Methylglucose ... 7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide 7,8-Dihydroxy-9,10-Epoxy-7,8,9,10-Tetrahydrobenzo(a)pyrene use 7,8-Dihydro-7 ... 2-Amino-5-phosphonovaleric Acid use 2-Amino-5-phosphonovalerate 2-Amino-6-(1,2,3-trihydroxypropyl)-4(3H)-pteridinone use ... 2-Dehydro-3-Deoxyphosphoheptonate Aldolase use 3-Deoxy-7-Phosphoheptulonate Synthase 2-Fluoro-2-deoxy-D-glucose use ...
3-methylglutaconicaciduria type II use Barth Syndrome 3-Methylindole use Skatole 3-O-Methyl-D-Glucose use 3-O-Methylglucose ... 7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide 7,8-Dihydroxy-9,10-Epoxy-7,8,9,10-Tetrahydrobenzo(a)pyrene use 7,8-Dihydro-7 ... 2-Amino-5-phosphonovaleric Acid use 2-Amino-5-phosphonovalerate 2-Amino-6-(1,2,3-trihydroxypropyl)-4(3H)-pteridinone use ... 2-Dehydro-3-Deoxyphosphoheptonate Aldolase use 3-Deoxy-7-Phosphoheptulonate Synthase 2-Fluoro-2-deoxy-D-Glucose use ...
3-methylglutaconicaciduria type II use Barth Syndrome 3-Methylindole use Skatole 3-O-Methyl-D-Glucose use 3-O-Methylglucose ... 7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide 7,8-Dihydroxy-9,10-Epoxy-7,8,9,10-Tetrahydrobenzo(a)pyrene use 7,8-Dihydro-7 ... 2-Amino-5-phosphonovaleric Acid use 2-Amino-5-phosphonovalerate 2-Amino-6-(1,2,3-trihydroxypropyl)-4(3H)-pteridinone use ... 2-Dehydro-3-Deoxyphosphoheptonate Aldolase use 3-Deoxy-7-Phosphoheptulonate Synthase 2-Fluoro-2-deoxy-D-Glucose use ...
3-methylglutaconicaciduria type II use Barth Syndrome 3-Methylindole use Skatole 3-O-Methyl-D-Glucose use 3-O-Methylglucose ... 7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide 7,8-Dihydroxy-9,10-Epoxy-7,8,9,10-Tetrahydrobenzo(a)pyrene use 7,8-Dihydro-7 ... 2-Amino-5-phosphonovaleric Acid use 2-Amino-5-phosphonovalerate 2-Amino-6-(1,2,3-trihydroxypropyl)-4(3H)-pteridinone use ... 2-Dehydro-3-Deoxyphosphoheptonate Aldolase use 3-Deoxy-7-Phosphoheptulonate Synthase 2-Fluoro-2-deoxy-D-glucose use ...
3-methylglutaconicaciduria type II use Barth Syndrome 3-Methylindole use Skatole 3-O-Methyl-D-Glucose use 3-O-Methylglucose ... 7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide 7,8-Dihydroxy-9,10-Epoxy-7,8,9,10-Tetrahydrobenzo(a)pyrene use 7,8-Dihydro-7 ... 2-Amino-5-phosphonovaleric Acid use 2-Amino-5-phosphonovalerate 2-Amino-6-(1,2,3-trihydroxypropyl)-4(3H)-pteridinone use ... 2-Dehydro-3-Deoxyphosphoheptonate Aldolase use 3-Deoxy-7-Phosphoheptulonate Synthase 2-Fluoro-2-deoxy-D-glucose use ...
7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide 7,8-Dihydroxy-9,10-Epoxy-7,8,9,10-Tetrahydrobenzo(a)pyrene use 7,8-Dihydro-7 ... 2-Amino-5-phosphonovaleric Acid use 2-Amino-5-phosphonovalerate 2-Amino-6-(1,2,3-trihydroxypropyl)-4(3H)-pteridinone use ... 2-Dehydro-3-Deoxyphosphoheptonate Aldolase use 3-Deoxy-7-Phosphoheptulonate Synthase 2-Fluoro-2-deoxy-D-glucose use ... 2,6-Dichlorophenolindophenol use 2,6-Dichloroindophenol 3 beta-Hydroxy-delta-5-Steroid Dehydrogenase use Progesterone Reductase ...
7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide 7,8-Dihydroxy-9,10-Epoxy-7,8,9,10-Tetrahydrobenzo(a)pyrene use 7,8-Dihydro-7 ... 2-Amino-5-phosphonovaleric Acid use 2-Amino-5-phosphonovalerate 2-Amino-6-(1,2,3-trihydroxypropyl)-4(3H)-pteridinone use ... 2-Dehydro-3-Deoxyphosphoheptonate Aldolase use 3-Deoxy-7-Phosphoheptulonate Synthase 2-Fluoro-2-deoxy-D-glucose use ... 2,6-Dichlorophenolindophenol use 2,6-Dichloroindophenol 3 beta-Hydroxy-delta-5-Steroid Dehydrogenase use Progesterone Reductase ...
3-methylglutaconicaciduria type II use Barth Syndrome 3-Methylindole use Skatole 3-O-Methyl-D-Glucose use 3-O-Methylglucose ... 7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide 7,8-Dihydroxy-9,10-Epoxy-7,8,9,10-Tetrahydrobenzo(a)pyrene use 7,8-Dihydro-7 ... 2-Amino-5-phosphonovaleric Acid use 2-Amino-5-phosphonovalerate 2-Amino-6-(1,2,3-trihydroxypropyl)-4(3H)-pteridinone use ... 2-Dehydro-3-Deoxyphosphoheptonate Aldolase use 3-Deoxy-7-Phosphoheptulonate Synthase 2-Fluoro-2-deoxy-D-Glucose use ...
7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide 7,8-Dihydroxy-9,10-Epoxy-7,8,9,10-Tetrahydrobenzo(a)pyrene use 7,8-Dihydro-7 ... 2-Amino-5-phosphonovaleric Acid use 2-Amino-5-phosphonovalerate 2-Amino-6-(1,2,3-trihydroxypropyl)-4(3H)-pteridinone use ... 2-Dehydro-3-Deoxyphosphoheptonate Aldolase use 3-Deoxy-7-Phosphoheptulonate Synthase 2-Fluoro-2-deoxy-D-glucose use ... 2,6-Dichlorophenolindophenol use 2,6-Dichloroindophenol 3 beta-Hydroxy-delta-5-Steroid Dehydrogenase use Progesterone Reductase ...
3-methylglutaconicaciduria type II use Barth Syndrome 3-Methylindole use Skatole 3-O-Methyl-D-Glucose use 3-O-Methylglucose ... 7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide 7,8-Dihydroxy-9,10-Epoxy-7,8,9,10-Tetrahydrobenzo(a)pyrene use 7,8-Dihydro-7 ... 2-Amino-5-phosphonovaleric Acid use 2-Amino-5-phosphonovalerate 2-Amino-6-(1,2,3-trihydroxypropyl)-4(3H)-pteridinone use ... 2-Dehydro-3-Deoxyphosphoheptonate Aldolase use 3-Deoxy-7-Phosphoheptulonate Synthase 2-Fluoro-2-deoxy-D-Glucose use ...
3-methylglutaconicaciduria type II use Barth Syndrome 3-Methylindole use Skatole 3-O-Methyl-D-Glucose use 3-O-Methylglucose ... 7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide 7,8-Dihydroxy-9,10-Epoxy-7,8,9,10-Tetrahydrobenzo(a)pyrene use 7,8-Dihydro-7 ... 2-Amino-5-phosphonovaleric Acid use 2-Amino-5-phosphonovalerate 2-Amino-6-(1,2,3-trihydroxypropyl)-4(3H)-pteridinone use ... 2-Dehydro-3-Deoxyphosphoheptonate Aldolase use 3-Deoxy-7-Phosphoheptulonate Synthase 2-Fluoro-2-deoxy-D-glucose use ...
2-Fluoro-2-deoxyglucose use Fluorodeoxyglucose F18 2H-Benzo(a)quinolizin-2-ol, 2-Ethyl-1,3,4,6,7,11b-hexahydro-3-isobutyl-9,10- ... 7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide 7,8-Dihydroxy-9,10-Epoxy-7,8,9,10-Tetrahydrobenzo(a)pyrene use 7,8-Dihydro-7 ... 2-Amino-5-phosphonovaleric Acid use 2-Amino-5-phosphonovalerate 2-Amino-6-(1,2,3-trihydroxypropyl)-4(3H)-pteridinone use ... 2-Oxoisovalerate Dehydrogenase (Lipoamide) use 3-Methyl-2-Oxobutanoate Dehydrogenase (Lipoamide) 2-PAM Compounds use ...
Angiotensin (Ang) II (SD Ang II) and Sarcosine1 , Isoleucine8 -Ang II (SI Ang II) and their radioiodinated congeners binding to ... Among the 20 amino acids that make up proteins, threonine (Thr) and isoleucine (Ile) have two chiral carbons and thus have two ... Angiotensin II analogue and ß-arrestin biased agonist TRV027 (Sarcosine1 , d-Alanine8 -Angiotensin (Ang) II; SD Ang II), ... The replacement of L-isoleucine with Da-isoleucine also confirmed that the isoleucine residues involved in the ß-sheet ...
At least two uncontrolled studies have found increases in plasma oxytocin at orgasm - in both men and women.[99][100] Plasma ... Oxytocin is a peptide of nine amino acids (a nonapeptide) in the sequence cysteine-tyrosine-isoleucine-glutamine-asparagine- ... The two genes are believed to result from a gene duplication event; the ancestral gene is estimated to be about 500 million ... The two genes are usually located close to each other (less than 15,000 bases apart) on the same chromosome, and are ...
The non-peptide angiotensin II (AII) receptor subtype selective antagonist, DuP 753, was used to characterize AII receptor ... Non-peptide angiotensin II receptor antagonists discriminate subtypes of 125I-angiotensin II binding sites in the rat brain. ... Angiotensin II receptor subtypes in the rat brain B P Rowe 1 , K L Grove, D L Saylor, R C Speth ... Angiotensin II receptor subtypes in the rat brain B P Rowe et al. Eur J Pharmacol. 1990. . ...
7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide 7,8-Dihydroxy-9,10-Epoxy-7,8,9,10-Tetrahydrobenzo(a)pyrene use 7,8-Dihydro-7 ... 2-Amino-5-phosphonovaleric Acid use 2-Amino-5-phosphonovalerate 2-Amino-6-(1,2,3-trihydroxypropyl)-4(3H)-pteridinone use ... 2-Dehydro-3-Deoxyphosphoheptonate Aldolase use 3-Deoxy-7-Phosphoheptulonate Synthase 2-Fluoro-2-deoxy-D-glucose use ... 2,6-Dichlorophenolindophenol use 2,6-Dichloroindophenol 3 beta-Hydroxy-delta-5-Steroid Dehydrogenase use Progesterone Reductase ...
angiotensin I (1-7) (Supplementary Concept). *aprikalim (Supplementary Concept). *Atenolol (MeSH Term) ... 1-Sarcosine-8-Isoleucine Angiotensin II (MeSH Term). *2-(4-(2-carboxyethyl)phenethylamino)-5-N-ethylcarboxamidoadenosine ( ... 1-(1-acetyl-piperidine-4-yl)-3-adamantan-1-yl-urea (Supplementary Concept) ... L-proline, N2-((1S)-1-carboxy-3-phenylpropyl)-N6-((4-hydroxyphenyl)iminomethyl)-L-lysyl- (Supplementary Concept) ...
Sarcosine (1968-1974)/analogs & derivatives (1975-1979). Public MeSH Note. 91; was see under ANGIOTENSIN II 1980-90. History ... Angiotensin II (1966-1974)/analogs & derivatives (1975-1979). Glycine (1966-1967). Isoleucine (1966-1974)/analogs & derivatives ... Angiotensins [D12.644.456.073] * Angiotensin II [D12.644.456.073.041] * Angiotensin Amide [D12.644.456.073.041.050] ... Angiotensins [D23.469.050.050] * Angiotensin II [D23.469.050.050.050] * Angiotensin Amide [D23.469.050.050.050.050] ...
Sarcosine (1968-1974)/analogs & derivatives (1975-1979). Public MeSH Note. 91; was see under ANGIOTENSIN II 1980-90. History ... Angiotensin II (1966-1974)/analogs & derivatives (1975-1979). Glycine (1966-1967). Isoleucine (1966-1974)/analogs & derivatives ... Angiotensins [D12.644.456.073] * Angiotensin II [D12.644.456.073.041] * Angiotensin Amide [D12.644.456.073.041.050] ... Angiotensins [D23.469.050.050] * Angiotensin II [D23.469.050.050.050] * Angiotensin Amide [D23.469.050.050.050.050] ...
Angiotensin II (1966-1974)/analogs & derivatives (1975-1979). Glycine (1966-1967). Isoleucine (1966-1974)/analogs & derivatives ... Sarcosine (1968-1974)/analogs & derivatives (1975-1979). Public MeSH Note:. 91; was see under ANGIOTENSIN II 1980-90. ... An ANGIOTENSIN II analog which acts as a highly specific inhibitor of ANGIOTENSIN TYPE 1 RECEPTOR. ... An ANGIOTENSIN II analog which acts as a highly specific inhibitor of ANGIOTENSIN TYPE 1 RECEPTOR.. ...
Angiostatins N0000171050 Angiotensin Amide N0000171051 Angiotensin I N0000171047 Angiotensin II N0000171052 Angiotensin III ... Reticulum Calcium-Transporting ATPases N0000170214 Sarcosine N0000167884 Sarcosine Dehydrogenase N0000169064 Sarcosine Oxidase ... N0000006307 Isoflurane N0000006308 Isoflurophate N0000178808 Isoindoles N0000006312 Isoleucine N0000167786 Isoleucine-tRNA ... Angiotensin II N0000167982 11-beta-Hydroxysteroid Dehydrogenase Type 1 N0000167981 11-beta-Hydroxysteroid Dehydrogenase Type 2 ...
ISOLEUCINE ANGIOTENSIN II ANGIOTENSIN-CONVERTING ENZYME INHIBITOR ANGIOTENSIN-CONVERTING ENZYME INHIBITOR ANGIOTENSIN- ... ANTIRHEUMATIC ANGIOTENSIN I ANTI-INFLAMMATORY AGENTS, ANTIRHEUMATIC ANGIOTENSIN II ANTI-INFLAMMATORY AGENTS, ANTIRHEUMATIC ... CARDIOVASCULAR AGENTS ANGIOTENSIN AMIDE CARDIOVASCULAR AGENTS ANGIOTENSIN II CARDIOVASCULAR AGENTS ANISTREPLASE CARDIOVASCULAR ... EPOXYMETHA VASOCONSTRICTOR AGENTS ANGIOTENSIN AMIDE VASOCONSTRICTOR AGENTS ANGIOTENSIN II VASOCONSTRICTOR AGENTS ARGIPRESSIN ...
The octapeptide amide of bovine angiotensin II used to increase blood pressure by vasoconstriction. ... "Angiotensin Amide" is a descriptor in the National Library of Medicines controlled vocabulary thesaurus, MeSH (Medical Subject ... This graph shows the total number of publications written about "Angiotensin Amide" by people in this website by year, and ... Below are the most recent publications written about "Angiotensin Amide" by people in Profiles. ...
Sar1,Val5,Ala8)Angiotensin II use Saralasin (Z)-2-(p-(2-Chloro-1,2-Diphenylvinyl)phenoxy)triethylamine Citrate use Zuclomiphene ... 2D-DIGE use Two-Dimensional Difference Gel Electrophoresis 2H-1-Benzopyran-3,5,7-triol, 2-(3,4-dihydroxyphenyl)-3,4-dihydro-, ( ... 2-ME use Mercaptoethanol 2-N-Butyl-3-((2-(1H-tetrazol-5-yl)biphenyl-4-yl)methyl)-1,3-diazaspiro(4,4)non-1-en-4-one use ... 1H-2-Benzopyran-1-ones use Isocoumarins 1H-3-Benzazepine-7,8-diol, 2,3,4,5-tetrahydro-1-phenyl- use 2,3,4,5-Tetrahydro-7,8- ...
Angiotensin II Angiotensin II ,Angiotensin II Angiotensin II Receptor,Angiotensin II Receptor Angiotensin II, 1-(N- ... 8A-L-threonine-10A-L-isoleucine-30B-L-threonine-,Insulin (ox), 8A-L-threonine-10A-L-isoleucine-30B-L-threonine- Insulin A Chain ... Des Asp Angiotensin II Des Aspartyl Angiotensin II,Des Aspartyl Angiotensin II Des-Asp Angiotensin II,Des-Asp Angiotensin II ... angiotensin ,angiotensin angiotensin II,angiotensin II angiotensin converting enzyme,angiotensin converting enzyme antithrombin ...
Angiotensin II Angiotensin II ,Angiotensin II Angiotensin II Receptor,Angiotensin II Receptor Angiotensin II, 1-(N- ... 8A-L-threonine-10A-L-isoleucine-30B-L-threonine-,Insulin (ox), 8A-L-threonine-10A-L-isoleucine-30B-L-threonine- Insulin A Chain ... Des Asp Angiotensin II Des Aspartyl Angiotensin II,Des Aspartyl Angiotensin II Des-Asp Angiotensin II,Des-Asp Angiotensin II ... angiotensin ,angiotensin angiotensin II,angiotensin II angiotensin converting enzyme,angiotensin converting enzyme antithrombin ...
Angiotensin (Ang) II (SD Ang II) and Sarcosine1 , Isoleucine8 -Ang II (SI Ang II) and their radioiodinated congeners binding to ... However, the Fe (II)/α-KG DOs that have been developed and characterized are not sufficient. L-isoleucine dioxygenase (IDO) is ... Angiotensin II analogue and ß-arrestin biased agonist TRV027 (Sarcosine1 , d-Alanine8 -Angiotensin (Ang) II; SD Ang II), ... TRV027 and 125 I-SD Ang II had reduced affinity for the AT1 receptor compared with SI Ang II and 125 I-SI Ang II. Additionally ...
Ile(5)-angiotensin II Ile(5)-angiotensin II dizwitterion Ile-Ile Ile-tRNA(Ile) ... alpha-L-Fuc-(1->2)-beta-D-Gal-(1->4)-beta-D-GlcNAc-(1->3)-beta-D-Gal-(1->4)-beta-D-GlcNAc-(1->3)-beta-D-Gal-(1->4)-beta-D-Glc-( ... beta-D-galactosyl-(1->4)-beta-D-glucosyl-N-(hexacosanoyl)sphingosine beta-D-galactosyl-1,3-(N-acetyl-beta-D-glucosaminyl-1,6)-N ... N(2)-phenylacetyl-L-glutamine N(4)-\{N-acetyl-beta-D-glucosaminyl-(1->2)-alpha-D-mannosyl-(1->3)-[N-acetyl-beta-D-glucosaminyl ...
At least two uncontrolled studies have found increases in plasma oxytocin at orgasm - in both men and women.[99][100] Plasma ... Oxytocin is a peptide of nine amino acids (a nonapeptide) in the sequence cysteine-tyrosine-isoleucine-glutamine-asparagine- ... The two genes are believed to result from a gene duplication event; the ancestral gene is estimated to be about 500 million ... The two genes are usually located close to each other (less than 15,000 bases apart) on the same chromosome, and are ...
  • Saralasin is a competitive angiotensin II receptor antagonist with partial agonist activity. (wikipedia.org)
  • The aminopeptide sequence for saralasin differs from angiotensin II at three sites. (wikipedia.org)
  • The non-peptide angiotensin II (AII) receptor subtype selective antagonist, DuP 753, was used to characterize AII receptor binding sites in the rat brain. (nih.gov)
  • Discrimination of angiotensin II receptor subtype distribution in the rat brain using non-peptidic receptor antagonists. (nih.gov)
  • Analysis of angiotensin II receptor subtypes in individual rat brain nuclei. (nih.gov)
  • Mapping of angiotensin II receptor subtype heterogeneity in rat brain. (nih.gov)
  • Non-peptide angiotensin II receptor antagonists discriminate subtypes of 125I-angiotensin II binding sites in the rat brain. (nih.gov)
  • Saralasin is a competitive angiotensin II receptor antagonist with partial agonist activity. (wikipedia.org)
  • An ANGIOTENSIN II analog which acts as a highly specific inhibitor of ANGIOTENSIN TYPE 1 RECEPTOR . (nih.gov)
  • Análogo de la ANGIOTENSINA II que actúa como inhibidor muy especíifico del RECEPTOR DE ANGIOTENSINA TIPO 1. (bvsalud.org)
  • PET imaging of the glucagon-like peptide-1 receptor (GLP-1R) using radiolabeled exendin is a promising imaging method to detect insulinomas. (bvsalud.org)
  • At position 5, isoleucine is replaced by valine, and at position 8, phenylalanine is replaced by alanine which leads to a smaller stimulatory effect. (wikipedia.org)
  • At position 1, sarcosine replaces aspartic acid increasing the affinity for vascular smooth muscle receptors and making the peptide resistant to degradation by aminopeptidases Pals et al (1979). (wikipedia.org)
  • The aminopeptide sequence for saralasin differs from angiotensin II at three sites. (wikipedia.org)
  • Angiotensin Amide" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings) . (uchicago.edu)
  • The octapeptide amide of bovine angiotensin II used to increase blood pressure by vasoconstriction. (uchicago.edu)
  • This graph shows the total number of publications written about "Angiotensin Amide" by people in this website by year, and whether "Angiotensin Amide" was a major or minor topic of these publications. (uchicago.edu)
  • Below are the most recent publications written about "Angiotensin Amide" by people in Profiles. (uchicago.edu)
  • The crystal heat capacities of the five N-acetyl amino acid amides were measured by Tian-Calvet calorimetry in the temperature interval (266-350 K), by power compensation DSC in the temperature interval (216-471 K), and by relaxation (heat-pulse) calorimetry in the temperature interval (2-268 K). As a result, reference heat capacities and thermodynamic functions for the crystalline phase from 0 K up to 470 K were developed. (bvsalud.org)
  • The 4-HIL titer of strains carrying PtacM-driven IleRS1 or IleRS3 (14.09 ± 1.07, 15.20 ± 0.93 g 4-HIL L-1) were similar with control strain S-D5I (15.73 ± 2.66 g 4-HIL L-1). (bvsalud.org)