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 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 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 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.
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.
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.
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.
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.
Cell surface proteins that bind ANGIOTENSINS and trigger intracellular changes influencing the behavior of cells.
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.
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.
An antagonist of ANGIOTENSIN TYPE 1 RECEPTOR with antihypertensive activity due to the reduced pressor effect of ANGIOTENSIN II.
Classic quantitative assay for detection of antigen-antibody reactions using a radioactively labeled substance (radioligand) either directly or indirectly to measure the binding of the unlabeled substance to a specific antibody or other receptor system. Non-immunogenic substances (e.g., haptens) can be measured if coupled to larger carrier proteins (e.g., bovine gamma-globulin or human serum albumin) capable of inducing antibody formation.
Liquid chromatographic techniques which feature high inlet pressures, high sensitivity, and high speed.
Body organ that filters blood for the secretion of URINE and that regulates ion concentrations.
PRESSURE of the BLOOD on the ARTERIES and other BLOOD VESSELS.
Partial proteins formed by partial hydrolysis of complete proteins or generated through PROTEIN ENGINEERING techniques.

The subtype 2 of angiotensin II receptors and pressure-natriuresis in adult rat kidneys. (1/383)

The present work examined the effects of the subtype 2 of angiotensin II (AT2) receptors on the pressure-natriuresis using a new peptide agonist, and the possible involvement of cyclic guanosine 3', 5' monophosphate (cyclic GMP) in these effects. In adult anaesthetized rats (Inactin, 100 mg kg(-1), i.p.) deprived of endogenous angiotensin II by angiotensin converting enzyme inhibition (quinapril, 10 mg kg(-1), i.v.), T2-(Ang II 4-8)2 (TA), a highly specific AT2 receptor agonist (5, 10 and 30 microg kg(-1) min(-1), i.v.) or its solvent was infused in four groups. Renal functions were studied at renal perfusion pressures (RPP) of 90, 110 and 130 mmHg and urinary cyclic GMP excretion when RPP was at 130 mmHg. The effects of TA (10 microg kg(-1) min(-1)) were reassessed in animals pretreated with PD 123319 (PD, 50 microg kg(-1) min(-1), i.v.), an AT2 receptor antagonist and the action of the same dose of PD alone was also determined. Increases in RPP from 90 to 130 mmHg did not change renal blood flow (RBF) but induced 8 and 15 fold increases in urinary flow and sodium excretion respectively. The 5 microg kg(-1) min(-1) dose of TA was devoid of action. The 10 and 30 microg kg(-1) min(-1) doses did not alter total RBF and glomerular filtration rate, but blunted pressure-diuresis and natriuresis relationships. These effects were abolished by PD. TA decreased urinary cyclic GMP excretion. After pretreatment with PD, this decrease was reversed to an increase which was also observed in animals receiving PD alone. In conclusion, renal AT2 receptors oppose the sodium and water excretion induced by acute increases in blood pressure and this action cannot be directly explained by changes in cyclic GMP.  (+info)

Cardiac growth factors in human hypertrophy. Relations with myocardial contractility and wall stress. (2/383)

The aim of the present study was to investigate whether and which cardiac growth factors are involved in human hypertrophy, whether growth factor synthesis is influenced by overload type and/or by the adequacy of the hypertrophy, and the relationships between cardiac growth factor formation and ventricular function. Cardiac growth factor formation was assessed by measuring aorta-coronary sinus concentration gradient in patients with isolated aortic stenosis (n=26) or regurgitation (n=15) and controls (n=12). Gene expression and cellular localization was investigated in ventricular biopsies using reverse transcriptase-polymerase chain reaction and in situ hybridization. Cardiac hypertrophy with end-systolic wall stress <90 kdyne/cm2 was associated with a selective increased formation of insulin-like growth factor (IGF)-I in aortic regurgitation and of IGF-I and endothelin (ET)-1 in aortic stenosis. mRNA levels for IGF-I and preproET-1 were elevated and mainly expressed in cardiomyocytes. At stepwise analysis, IGF-I formation was correlated to the mean velocity of circumferential fiber shortening (r=0.86, P<0.001) and ET-1 formation to relative wall thickness (r=0.82, P<0. 001). When end-systolic wall stress was >90 kdyne/cm2, IGF-I and ET-1 synthesis by cardiomyocytes was no longer detectable, and only angiotensin (Ang) II was generated, regardless of the type of overload. The mRNA level for angiotensinogen was high, and the mRNA was exclusively expressed in the interstitial cells. Ang II formation was positively correlated to end-systolic stress (r=0.89, P<0.001) and end-diastolic stress (r=0.84, P<0.001). Multivariate stepwise analysis selected end-systolic stress as the most predictive variable and left ventricular end-diastolic pressure as the independent variable for Ang II formation (r=0.93, P<0.001). In conclusion, the present results indicate that the course of human left ventricular hypertrophy is characterized by the participation of different cardiac growth factors that are selectively related both to the type of hemodynamic overload and to ventricular function.  (+info)

Angiotensin regulates the selectivity of the Na+-K+ pump for intracellular Na+. (3/383)

Treatment of rabbits with angiotensin-converting enzyme (ACE) inhibitors increases the apparent affinity of the Na+-K+ pump for Na+. To explore the mechanism, we voltage clamped myocytes from control rabbits and rabbits treated with captopril with patch pipettes containing 10 mM Na+. When pipette solutions were K+ free, pump current (Ip) for myocytes from captopril-treated rabbits was nearly identical to that for myocytes from controls. However, treatment caused a significant increase in Ip measured with pipettes containing K+. A similar difference was observed when myocytes from rabbits treated with the ANG II receptor antagonist losartan and myocytes from controls were compared. Treatment-induced differences in Ip were eliminated by in vitro exposure to ANG II or phorbol 12-myristate 13-acetate or inclusion of the protein kinase C fragment composed of amino acids 530-558 in pipette solutions. Treatment with captopril had no effect on the voltage dependence of Ip. We conclude that ANG II regulates the pump's selectivity for intracellular Na+ at sites near the cytoplasmic surface. Protein kinase C is implicated in the messenger cascade.  (+info)

Central lead administration inhibits water intake and sodium appetite in rats. (4/383)

We have demonstrated that acute third ventricle injections of lead acetate (PbAc) exert a powerful antidipsogenic effect and induce a significant increase in renal sodium excretion. In the present study we confirm the antidipsogenic effect of lead and demonstrate that central administration of this metal, in minute amounts, significantly reduces salt intake both during dehydration and after central angiotensinergic stimulation. Adult male Wistar rats had the third ventricle cannulated seven days before the experiments. During this period they had free access to distilled water and hypertonic saline solution (1.5%). After a 24-h period of fluid deprivation, experimental animals received third ventricle injections of PbAc (0.3, N = 8 and 3.0 nmol/rat, N = 14) while controls received sodium acetate (NaAc; 3.0 nmol/rat, N = 10). Rats treated with PbAc at the highest dose showed a significant reduction (P<0.05) both in water and hypertonic saline intake when compared to controls. When the effect of lead administration on angiotensin II-induced water and salt intake was studied, normohydrated animals received third ventricle injections of angiotensin II (9.6 nmol/rat) after pretreatment with 3.0 nmol/rat of PbAc (experimental group, N = 10) or NaAc (controls, N = 8). The group pretreated with PbAc presented a significant reduction (P<0.05) in both water and salt intake compared to controls. Thus, this study confirms the antidipsogenic effect of central lead injections and demonstrates that the presence of lead in the brain exerts a significant inhibition of sodium appetite.  (+info)

Self-protection by cardiac myocytes against hypoxia and hyperoxia. (5/383)

Cardiac muscle must maintain a continuous balance between its energy supply and work performed. An important mechanism involved in achievement of this balance is cross talk via chemical signals between cardiac myocytes and the cardiac muscle vascular system. This has been demonstrated by incubating isolated cardiac myocytes in different concentrations of oxygen and then assaying the conditioned media for vasoactive substances on isolated aortic rings and small-resistance arteries. With increasing oxygen concentrations above 6%, cardiac myocytes produce increasing amounts of angiotensin I, which is converted to angiotensin II by the blood vessel. The angiotensin II stimulates vascular endothelial cells to secrete endothelin and increase vascular tone. Below 6% oxygen, cardiac myocytes secrete adenosine, which acts directly on vascular smooth muscle to block the effect of alpha-adrenergic agonists and reduce vascular tone. In an intact heart, the net effect of these 2 regulatory systems would be the maintenance of oxygen concentration within a narrow range at the cardiac myocytes. By acting as oxygen sensors, cardiac myocytes modulate vascular tone according to the needs of the myocytes and reduce potential problems of hypoxia and extensive formation of reactive oxygen species.  (+info)

Regulated expression of human angiotensinogen gene by hepatocyte nuclear factor 4 and chicken ovalbumin upstream promoter-transcription factor. (6/383)

We previously identified various upstream and downstream regulatory elements and factors important for hepatic expression of the human angiotensinogen (ANG) gene, the precursor of vasoactive octapeptide angiotensin II. In the present study, to further investigate the molecular mechanism of human ANG transcriptional regulation, we generated transgenic mice carrying the fusion gene composed of the 1. 3-kilobase promoter of the human ANG gene, its downstream enhancer, and the chloramphenicol acetyltransferase reporter gene. Because expression of the chloramphenicol acetyltransferase gene was observed strongly in the liver and weakly in the kidney, we suspected that hepatocyte nuclear factor (HNF) 4 with a tissue expression pattern similar to that of the reporter gene would regulate ANG transcription. In vitro assays indicated that HNF4 bound to the promoter elements and strongly activated the ANG transcription, but that chicken ovalbumin upstream promoter transcription factor (COUP-TF), a transcriptional repressor, dramatically repressed human ANG transcription through the promoter elements and the downstream enhancer core elements. Furthermore, COUP-TF dramatically decreased the human ANG transcription in the mouse liver by the Helios Gene Gun system in vivo. These results suggest that an interplay between HNF4 and COUP-TF could be important in hepatic human ANG transcription.  (+info)

Evaluation of the angiotensin challenge methodology for assessing the pharmacodynamic profile of antihypertensive drugs acting on the renin-angiotensin system. (7/383)

AIMS: The performance of the experimental paradigm of angiotensin challenges with continuous non-invasive blood pressure measurement was evaluated. Angiotensin dose-response relationships were characterized, along with the influence of clinical covariates. The stability of angiotensin-induced peaks and the variability of the angiotensin doses were assessed. Finally, the predictive value of studies based on angiotensin challenges to determine drug doses effective in therapeutics was evaluated. METHODS: The data were gathered from 13 clinical studies on nine angiotensin II receptor antagonists, one ACE inhibitor and one dual ACE-NEP inhibitor, using Finapres for measuring the response to exogenous angiotensin challenges. Modelling of angiotensin dose-response curves and determination of the inter and intrasubject variability were performed by nonlinear regression (NONMEM). The different sources of variations in angiotensin I and II doses and angiotensin-induced peaks were evaluated by analyses of variance. The dose of ACE inhibitors and angiotensin II receptor antagonists inhibiting blood pressure increase by at least 75%, as measured by this method, was chosen for comparison with the labelled starting dose. RESULTS: Angiotensin challenges exhibited a clear dose-response relationship which can be characterized both by an Emax or a log linear model. The log linear model gave an average systolic/diastolic response of 24+/-6/20+/-5 mmHg for a unit dose of 1 microgram of angiotensin II equivalents, and an increase of 6/6 mmHg for each doubling of the dose. The angiotensin ED50 calculated values were 0.67 microgram for systolic and 0.84 microgram for diastolic blood pressure. The angiotensin doses for eliciting a given response and the angiotensin induced peaks were fairly constant between period and subject, but vary significantly between studies. Based on an inhibition of blood pressure by 75%, the agreement was good between the doses of ACE inhibitors and angiotensin receptor antagonists predicted from studies using the methodology of angiotensin challenges and the doses shown to be clinically efficacious, in spite of high intersubject and intrasubject variabilities. CONCLUSIONS: This experimental method represents a valid surrogate for the therapeutic target and a useful tool for the pharmacokinetic and pharmacodynamic profiling of drugs acting on the renin-angiotensin system.  (+info)

Angiotensin I-converting enzyme antisense gene therapy causes permanent antihypertensive effects in the SHR. (8/383)

The renin-angiotensin system plays a critical role in the control of blood pressure (BP), and its hyperactivity is associated with the development and maintenance of hypertension. Although traditional pharmacological therapies targeted toward the inhibition of the renin-angiotensin system are effective in the control of this disease, they pose significant limitations. We used an antisense gene delivery strategy to circumvent these limitations and established that a single intracardiac administration of angiotensin type 1 receptor antisense (AT(1)R-AS) causes permanent prevention of hypertension in the spontaneously hypertensive rat (SHR), an animal model of primary human hypertension. Our objectives in this study were 2-fold: to determine (1) whether the targeting of angiotensin I-converting enzyme (ACE) mRNA by a similar antisense strategy would prevent the SHR from developing hypertension and (2) whether the antihypertensive phenotype is transmitted to the offspring from the antisense-treated parents. Administration of a retroviral vector containing ACE antisense (LNSV-ACE-AS) caused a modest yet significant attenuation of high BP ( approximately 15+/-2 mm Hg) exclusively in the SHR. This was associated with a complete prevention of cardiac and renovascular pathophysiological alterations that are characteristic of hypertension. Like their parents, the F(1) generation offspring of the LNSV-ACE-AS-treated SHR expressed lower BP, decreased cardiac hypertrophy, and normalization of renal arterial excitation-coupling compared with offspring derived from the LNSV-ACE-tS (truncated sense)-treated SHR. In addition, the endothelial dysfunction commonly observed in the SHR renal arterioles was significantly prevented in both parents and offspring of the LNSV-ACE-AS-treated SHR. Polymerase chain reaction followed by Southern analysis revealed that the ACE-AS was integrated into the SHR genome and transmitted to the offspring. These observations suggest that transmission of ACE-AS by retroviral vector may be responsible for the transference of normotensive phenotypes in the SHR offspring.  (+info)

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.

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.

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.

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.

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."

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.

The Renin-Angiotensin System (RAS) is a complex hormonal system that regulates blood pressure, fluid and electrolyte balance, and vascular resistance. It plays a crucial role in the pathophysiology of hypertension, heart failure, and kidney diseases.

Here's a brief overview of how it works:

1. Renin is an enzyme that is released by the juxtaglomerular cells in the kidneys in response to decreased blood pressure or reduced salt delivery to the distal tubules.
2. Renin acts on a protein called angiotensinogen, which is produced by the liver, converting it into angiotensin I.
3. Angiotensin-converting enzyme (ACE), found in the lungs and other tissues, then converts angiotensin I into angiotensin II, a potent vasoconstrictor that narrows blood vessels and increases blood pressure.
4. Angiotensin II also stimulates the release of aldosterone from the adrenal glands, which promotes sodium and water reabsorption in the kidneys, further increasing blood volume and blood pressure.
5. Additionally, angiotensin II has direct effects on the heart, promoting hypertrophy and remodeling, which can contribute to heart failure.
6. The RAS can be modulated by various medications, such as ACE inhibitors, angiotensin receptor blockers (ARBs), and aldosterone antagonists, which are commonly used to treat hypertension, heart failure, and kidney diseases.

Angiotensinogen is a protein that is produced mainly by the liver. It is the precursor to angiotensin I, which is a molecule that begins the process of constriction (narrowing) of blood vessels, leading to an increase in blood pressure. When angiotensinogen comes into contact with an enzyme called renin, it is cleaved into angiotensin I. Angiotensin-converting enzyme (ACE) then converts angiotensin I into angiotensin II, which is a potent vasoconstrictor and a key player in the body's regulation of blood pressure and fluid balance.

Angiotensinogen is an important component of the renin-angiotensin-aldosterone system (RAAS), which helps to regulate blood pressure and fluid balance by controlling the volume and flow of fluids in the body. Disorders of the RAAS can lead to high blood pressure, kidney disease, and other health problems.

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-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.

Captopril is a medication that belongs to a class of drugs called ACE (angiotensin-converting enzyme) inhibitors. It works by blocking the action of a chemical in the body called angiotensin II, which causes blood vessels to narrow and release hormones that can increase blood pressure. By blocking the action of angiotensin II, captopril helps relax and widen blood vessels, which lowers blood pressure and improves blood flow.

Captopril is used to treat high blood pressure (hypertension), congestive heart failure, and to improve survival after a heart attack. It may also be used to protect the kidneys from damage due to diabetes or high blood pressure. The medication comes in the form of tablets that are taken by mouth, usually two to three times per day.

Common side effects of captopril include cough, dizziness, headache, and skin rash. More serious side effects may include allergic reactions, kidney problems, and changes in blood cell counts. It is important for patients taking captopril to follow their doctor's instructions carefully and report any unusual symptoms or side effects promptly.

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."

Radioimmunoassay (RIA) is a highly sensitive analytical technique used in clinical and research laboratories to measure concentrations of various substances, such as hormones, vitamins, drugs, or tumor markers, in biological samples like blood, urine, or tissues. The method relies on the specific interaction between an antibody and its corresponding antigen, combined with the use of radioisotopes to quantify the amount of bound antigen.

In a typical RIA procedure, a known quantity of a radiolabeled antigen (also called tracer) is added to a sample containing an unknown concentration of the same unlabeled antigen. The mixture is then incubated with a specific antibody that binds to the antigen. During the incubation period, the antibody forms complexes with both the radiolabeled and unlabeled antigens.

After the incubation, the unbound (free) radiolabeled antigen is separated from the antibody-antigen complexes, usually through a precipitation or separation step involving centrifugation, filtration, or chromatography. The amount of radioactivity in the pellet (containing the antibody-antigen complexes) is then measured using a gamma counter or other suitable radiation detection device.

The concentration of the unlabeled antigen in the sample can be determined by comparing the ratio of bound to free radiolabeled antigen in the sample to a standard curve generated from known concentrations of unlabeled antigen and their corresponding bound/free ratios. The higher the concentration of unlabeled antigen in the sample, the lower the amount of radiolabeled antigen that will bind to the antibody, resulting in a lower bound/free ratio.

Radioimmunoassays offer high sensitivity, specificity, and accuracy, making them valuable tools for detecting and quantifying low levels of various substances in biological samples. However, due to concerns about radiation safety and waste disposal, alternative non-isotopic immunoassay techniques like enzyme-linked immunosorbent assays (ELISAs) have become more popular in recent years.

High-performance liquid chromatography (HPLC) is a type of chromatography that separates and analyzes compounds based on their interactions with a stationary phase and a mobile phase under high pressure. The mobile phase, which can be a gas or liquid, carries the sample mixture through a column containing the stationary phase.

In HPLC, the mobile phase is a liquid, and it is pumped through the column at high pressures (up to several hundred atmospheres) to achieve faster separation times and better resolution than other types of liquid chromatography. The stationary phase can be a solid or a liquid supported on a solid, and it interacts differently with each component in the sample mixture, causing them to separate as they travel through the column.

HPLC is widely used in analytical chemistry, pharmaceuticals, biotechnology, and other fields to separate, identify, and quantify compounds present in complex mixtures. It can be used to analyze a wide range of substances, including drugs, hormones, vitamins, pigments, flavors, and pollutants. HPLC is also used in the preparation of pure samples for further study or use.

A kidney, in medical terms, is one of two bean-shaped organs located in the lower back region of the body. They are essential for maintaining homeostasis within the body by performing several crucial functions such as:

1. Regulation of water and electrolyte balance: Kidneys help regulate the amount of water and various electrolytes like sodium, potassium, and calcium in the bloodstream to maintain a stable internal environment.

2. Excretion of waste products: They filter waste products from the blood, including urea (a byproduct of protein metabolism), creatinine (a breakdown product of muscle tissue), and other harmful substances that result from normal cellular functions or external sources like medications and toxins.

3. Endocrine function: Kidneys produce several hormones with important roles in the body, such as erythropoietin (stimulates red blood cell production), renin (regulates blood pressure), and calcitriol (activated form of vitamin D that helps regulate calcium homeostasis).

4. pH balance regulation: Kidneys maintain the proper acid-base balance in the body by excreting either hydrogen ions or bicarbonate ions, depending on whether the blood is too acidic or too alkaline.

5. Blood pressure control: The kidneys play a significant role in regulating blood pressure through the renin-angiotensin-aldosterone system (RAAS), which constricts blood vessels and promotes sodium and water retention to increase blood volume and, consequently, blood pressure.

Anatomically, each kidney is approximately 10-12 cm long, 5-7 cm wide, and 3 cm thick, with a weight of about 120-170 grams. They are surrounded by a protective layer of fat and connected to the urinary system through the renal pelvis, ureters, bladder, and urethra.

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.

A peptide fragment is a short chain of amino acids that is derived from a larger peptide or protein through various biological or chemical processes. These fragments can result from the natural breakdown of proteins in the body during regular physiological processes, such as digestion, or they can be produced experimentally in a laboratory setting for research or therapeutic purposes.

Peptide fragments are often used in research to map the structure and function of larger peptides and proteins, as well as to study their interactions with other molecules. In some cases, peptide fragments may also have biological activity of their own and can be developed into drugs or diagnostic tools. For example, certain peptide fragments derived from hormones or neurotransmitters may bind to receptors in the body and mimic or block the effects of the full-length molecule.

It is cleaved at the N-terminus by renin to result in angiotensin I, which will later be modified to become angiotensin II. ... It is part of the renin-angiotensin system, which regulates blood pressure. Angiotensin also stimulates the release of ... An oligopeptide, angiotensin is a hormone and a dipsogen. It is derived from the precursor molecule angiotensinogen, a serum ... Angiotensinogen is an α-2-globulin synthesized in the liver and is a precursor for angiotensin, but has also been indicated as ...
Proteopedia Angiotensin-converting_enzyme - the Angiotensin-Converting Enzyme Structure in Interactive 3D Angiotensin+ ... Angiotensin II binds to the type 1 angiotensin II receptor (AT1), which sets off a number of actions that result in ... Angiotensin-converting enzyme (EC 3.4.15.1), or ACE, is a central component of the renin-angiotensin system (RAS), which ... In addition, inhibiting angiotensin II formation diminishes angiotensin II-mediated aldosterone secretion from the adrenal ...
The decapeptide is known as angiotensin I. Angiotensin I is then converted to an octapeptide, angiotensin II by angiotensin- ... Angiotensin I may have some minor activity, but angiotensin II is the major bio-active product. Angiotensin II has a variety of ... Angiotensin II receptor antagonists, also known as angiotensin receptor blockers, can be used to prevent angiotensin II from ... Angiotensin I is subsequently converted to angiotensin II (an octapeptide) by the angiotensin-converting enzyme (ACE) found on ...
The angiotensin II receptors, (ATR1) and (ATR2), are a class of G protein-coupled receptors with angiotensin II as their ... The angiotensin receptor is activated by the vasoconstricting peptide angiotensin II. The activated receptor in turn couples to ... The AT4 receptor is activated by the angiotensin II metabolite angiotensin IV, and may play a role in regulation of the CNS ... angiotensin II. The AT1 and AT2 receptors share a sequence identity of ~30%, but have a similar affinity for angiotensin II, ...
2018). "The ACE2/Angiotensin-(1-7)/MAS Axis of the Renin-Angiotensin System: Focus on Angiotensin-(1-7)". Physiol Rev. 1 (98): ... Action of neprilysin on angiotensin I or angiotensin II. Action of prolyl endopeptidase on angiotensin I. Action of ACE on ... angiotensin 1-9. Action of neprilysin on angiotensin 1-9. Action of ACE2 on angiotensin II. Ang (1-7) has been shown to have ... Santos et al demonstrated that angiotensin (1-7) was a main product of the incubation of angiotensin I with brain micropunches ...
Angiotensin II receptor blockers, as their name implies, block the action of angiotensin II at its receptors and therefore may ... Angiotensin II is a naturally occurring hormone secreted as part of the renin-angiotensin system that results in powerful ... Angiotensin II is as a treatment option that can increase blood pressure and allow catecholamine dose reductions. Angiotensin ... "Angiotensin II". Drug Information Portal. U.S. National Library of Medicine. "Angiotensin II acetate". Drug Information Portal ...
September 2000). "A novel angiotensin-converting enzyme-related carboxypeptidase (ACE2) converts angiotensin I to angiotensin 1 ... March 2020). "Angiotensin II and angiotensin 1-7: which is their role in atrial fibrillation?". Heart Failure Reviews. Springer ... It is released into the bloodstream where one of sACE2's functions is to turn excess angiotensin II into angiotensin 1-7 which ... ACE2 has an opposing effect to ACE, degrading angiotensin II into angiotensin (1-7), thereby lowering blood pressure. sACE2, as ...
While angiotensin converting enzyme (ACE) inhibitors block the cleavage of angiotensin I to angiotensin II, the active peptide ... Angiotensin II receptor blockers (ARBs), formally angiotensin II receptor type 1 (AT1) antagonists, also known as angiotensin ... "Angiotensin FDA Drug Safety Communication: No increase in risk of cancer with certain blood pressure drugs - Angiotensin ... "List of Angiotensin receptor blockers (angiotensin II inhibitors)". Drugs.com. 2020-02-28. Retrieved 2020-03-21. "Blood ...
... (AT1) is the best characterized angiotensin receptor. It is encoded in humans by the AGTR1 gene ... The angiotensin receptor is activated by the vasoconstricting peptide angiotensin II. The activated receptor in turn couples to ... "Angiotensin II receptor blocker", Wikipedia, 2022-07-26, retrieved 2022-08-10 Wilson JX (1984). "The renin-angiotensin system ... shows considerably less binding affinities in case of all angiotensin receptor blockers (ARBs). Angiotensin II receptor type 1 ...
... has been shown to interact with MTUS1. Angiotensin II receptor GRCh38: Ensembl release 89: ... "The angiotensin II type 2 receptor causes constitutive growth of cardiomyocytes and does not antagonize angiotensin II type 1 ... Angiotensin II receptor type 2, also known as the AT2 receptor is a protein that in humans is encoded by the AGTR2 gene. ... "Entrez Gene: AGTR2 angiotensin II receptor, type 2". Ewert S, Laesser M, Johansson B, Holm M, Aneman A, Fandriks L (March 2003 ...
The angiotensin receptor blockers (ARBs), also called angiotensin (AT1) receptor antagonists or sartans, are a group of ... "The distribution of angiotensin II type 1 receptors, and the tissue renin-angiotensin systems", Molecular Medicine Today, 1 (1 ... Renin and Angiotensin; Jackson E.K., 789-821) Editors; Brunton L.L., Lazo J.S., Parker K.L. New York McGraw Hill 2006. ISBN 0- ... Two more angiotensin receptors have been described, AT3 and AT4, but their role is still unknown. AT1 receptors are mainly ...
... is a peer-reviewed academic journal that publishes papers in the field of ... Journal of the Renin-Angiotensin-Aldosterone System is abstracted and indexed in, among other databases: SCOPUS, and the Social ... Journal of the Renin-Angiotensin-Aldosterone System is a resource for biomedical professionals, including basic scientists and ... Journal of the Renin-Angiotensin-Aldosterone System also publishes research on other peptides, such as vasopressin, the ...
It is a derivative of angiotensin II. Angiotensin "Angiotensinamide". Index nominum, international drug directory = ... Angiotensinamide (INN; BAN and USAN angiotensin amide) is a potent vasoconstrictor used as a cardiac stimulant. ...
Angiotensin II -> Vasopressin) Increase PAI-1 and PAI-2 also through Angiotensin II Lipid Increase HDL, triglyceride Decrease ...
The production of aldosterone is regulated via the renin-angiotensin II-aldosterone system, a system composed of baroreceptors ... Fountain JH, Kaur J, Lappin SL (2023). "Physiology, Renin Angiotensin System". StatPearls. Treasure Island (FL): StatPearls ...
The conversion of angiotensin I to angiotensin II and the inactivation of bradykinin were thought to be mediated by the same ... The first breakthrough was made by Kevin K.F. Ng in 1967, when he found the conversion of angiotensin I to angiotensin II took ... Ng KK, Vane JR (November 1967). "Conversion of angiotensin I to angiotensin II". Nature. 216 (5117): 762-766. Bibcode:1967Natur ... Captopril blocks the conversion of angiotensin I to angiotensin II and prevents the degradation of vasodilatory prostaglandins ...
e.g., angiotensin IV). A heptapeptide has seven amino acids. (e.g., spinorphin). An octapeptide has eight amino acids (e.g., ... angiotensin II). A nonapeptide has nine amino acids (e.g., oxytocin). A decapeptide has ten amino acids (e.g., gonadotropin- ... releasing hormone and angiotensin I). A undecapeptide has eleven amino acids (e.g., substance P). The same words are also used ...
... which is converted by angiotensin converting enzyme to angiotensin II. Angiotensin II then signals to the adrenal cortex to ... Renin converts angiotensinogen (inactive form) to angiotensin I (active form). Angiotensin I flows in the bloodstream until it ... acts on it to convert it into angiotensin II. Angiotensin II is a vasoconstrictor that will increase blood flow to the heart ... Renin-angiotensin system (RAS): This system is generally known for its long-term adjustment of arterial pressure. This system ...
Angiotensin blockers were created in order to avoid the side effects of ACE inhibitors, which were previously the drug of ... In addition, his work on angiotensin blockers has helped many patients in need of treatment for congestive heart failure, even ... Watkins left Johns Hopkins in 1973 for Harvard University where he researched the use of angiotensin blockers in cases of ... Two years after his research on angiotensin blockers at Harvard, Watkins returned to Johns Hopkins and joined the admissions ...
Angiotensin-converting-enzyme; ARB = Angiotensin-receptor-blocker). Afterload also increases with increasing blood viscosity, ...
... preventing angiotensin I from being converted to angiotensin II. Angiotensin II is a potent direct vasoconstrictor and a ... Khan MG (2015). "Angiotensin-Converting Enzyme Inhibitors and Angiotensin II Receptor Blockers". Cardiac Drug Therapy. New York ... Reduction in the amount of angiotensin II results in relaxation of the arterioles. Reduction in the amount of angiotensin II ... Lisinopril is an ACE inhibitor, meaning it blocks the actions of angiotensin-converting enzyme (ACE) in the renin-angiotensin- ...
Reilly CF, Tewksbury DA, Schechter NM, Travis J (August 1982). "Rapid conversion of angiotensin I to angiotensin II by ... Other functions of cathepsin G have been reported, including cleavage of receptors, conversion of angiotensin I to angiotensin ... Klickstein LB, Kaempfer CE, Wintroub BU (December 1982). "The granulocyte-angiotensin system. Angiotensin I-converting activity ...
Medical treatment involves use of an angiotensin-converting enzyme inhibitor (ACEi) or an angiotensin receptor blocker (ARB) to ... The elevated blood pressure seen in Page kidney is thought to be caused by the activation of the renin-angiotensin-aldosterone ... The compression is believed to cause activation of the renin-angiotensin-aldosterone system (RAAS) via microvascular ischemia.[ ... In this case, medical treatment focuses on symptomatic treatment of the hypertension with an angiotensin-converting enzyme ...
Ryan, Una; Ryan, James W (April 1980). "Angiotensin-Converting Enzyme: II. Pulmonary Endothelial Cells in Culture". ... taking up a Howard Hughes Fellowship at the University of Miami to study angiotensin-converting enzymes. After completion of ...
Use of angiotensin-converting enzyme (ACE) inhibitors (ACE-I), or angiotensin receptor blockers (ARB) if the person develops a ... Inhibitors of the renin-angiotensin system (RAS) are recommended in heart failure. The angiotensin receptor-neprilysin ... In heart failure due to left ventricular dysfunction, angiotensin-converting-enzyme inhibitors, angiotensin receptor blockers, ... Vasopressin levels are usually increased, along with renin, angiotensin II, and catecholamines to compensate for reduced ...
Angiotensin-converting enzyme (ACE) then catalyzes the reaction that forms angiotensin II, which acts on AT1 receptors on the ... Harada K, Sugaya T, Murakami K, Yazaki Y, Komuro I (November 1999). "Angiotensin II type 1A receptor knockout mice display less ... Sun Y, Zhang JQ, Zhang J, Ramires FJ (August 1998). "Angiotensin II, transforming growth factor-beta1 and repair in the ... Fimasartan is a non-peptide angiotensin II receptor antagonist (ARB) used for the treatment of hypertension and heart failure. ...
ACE inhibitor Angiotensin conversion enzyme. A class of drugs used to decrease hypertension, mainly by interfering with the ... Insulin is a hormone as are glucagon, adrenaline, and angiotensin II. Human insulin Man-made insulins that is identical to the ...
... angiotensin converting enzyme (ACE, CD143); tissue factor TF (CD142, thromboplastin); decay accelerating factor (CD55); ...
Ruilope LM, Tamargo J (April 2017). "Renin-angiotensin system blockade: Finerenone". Nephrologie & Therapeutique. 13 Suppl 1: ...
Inagaki K, Iwanaga Y, Sarai N, Onozawa Y, Takenaka H, Mochly-Rosen D, Kihara Y (Oct 2002). "Tissue angiotensin II during ... Paul K, Ball NA, Dorn GW, Walsh RA (Nov 1997). "Left ventricular stretch stimulates angiotensin II--mediated ... angiotensin II and diastolic stretch; adenosine; hypoxia and Akt-induced stem cell factor; ROS generated via pharmacologic ...
It is cleaved at the N-terminus by renin to result in angiotensin I, which will later be modified to become angiotensin II. ... It is part of the renin-angiotensin system, which regulates blood pressure. Angiotensin also stimulates the release of ... An oligopeptide, angiotensin is a hormone and a dipsogen. It is derived from the precursor molecule angiotensinogen, a serum ... Angiotensinogen is an α-2-globulin synthesized in the liver and is a precursor for angiotensin, but has also been indicated as ...
SARS-CoV-2 gains cell entry via angiotensin-converting enzyme (ACE) 2, a membrane-bound enzyme of the ... Ratio of angiotensin II to angiotensin I (A, B) The ratio of angiotensin II to angiotensin I (ALT-S) was reduced in severe ... The equilibrium levels of six angiotensin peptide metabolites (angiotensins I-IV, angiotensin 1-7, angiotensin 1-5) in human ... drives angiotensin II formation from angiotensin I, ACE2 opposes its action through conversion of angiotensin II to angiotensin ...
The decapeptide is known as angiotensin I.. *Angiotensin I is then converted to an octapeptide, angiotensin II by angiotensin- ... Angiotensin I may have some minor activity, but angiotensin II is the major bio-active product. Angiotensin II has a variety of ... Angiotensin II receptor antagonists, also known as angiotensin receptor blockers, can be used to prevent angiotensin II from ... Angiotensin I is subsequently converted to angiotensin II (an octapeptide) by the angiotensin-converting enzyme (ACE) found on ...
The American Academy of Anti-Aging Medicine features anti-aging health tips, latest health news, and anti-aging research in regenerative and functional medicine
There was no evidence of the benefit when comparing angiotensin receptor blockers with angiotensin-converting enzyme inhibitors ... Evidence of the benefit of angiotensin receptor blockers on the risk of stroke is provided when compared with placebo. ... There was no evidence of the benefit when comparing angiotensin receptor blockers with angiotensin-converting enzyme inhibitors ... Angiotensin receptor blockers were associated with no significant reduction in the risk of stroke compared with angiotensin- ...
... particularly in models involving angiotensin II (Ang II). We tested the hypothesis that ER stress in the brain is causally ...
Angiotensin-converting enzyme inhibitors (ACEi) are commonly used for pediatric cardiology patients. However, studies examining ... Angiotensin-converting enzyme inhibitor nephrotoxicity in neonates with cardiac disease Pediatr Cardiol. 2014 Mar;35(3):499-506 ... Angiotensin-converting enzyme inhibitors (ACEi) are commonly used for pediatric cardiology patients. However, studies examining ...
Initial Dosage Regimens for Angiotensin-Converting Enzyme Inhibitors. ACE (angiotensin converting enzyme) inhibitors inhibit ... Cardiovascular risk reduction in hypertension: angiotensin-converting enzyme inhibitors, angiotensin receptor blockers. Where ... Health outcomes and economic consequences of using angiotensin-converting enzyme inhibitors in comparison with angiotensin ... Angiotensin-Converting Enzyme Inhibitors in Hypertension: To Use or Not to Use?. J Am Coll Cardiol. 2018 Apr 3. 71 (13):1474- ...
has prepared and tested new angiotensin AT1 receptor (AGTR1) antagonists reported to be useful for the treatment of cancer, ... has prepared and tested new angiotensin AT1 receptor (AGTR1) antagonists reported to be useful for the treatment of cancer, ...
Centrifuge refrigerated within 1 hour of collection. Separate serum from clot. EDTA is not acceptable.. ...
The observation was then made by Vane that these peptides could also block the conversion of angiotensin I into angiotensin II ... and to block totally the conversion of angiotensin I into angiotensin II.20 Therefore, the clinical importance of the escape ... The angiotensin-converting-enzyme inhibition in progressive renal insufficiency study group. Kidney Int Suppl 63:S63-S66. ... Also, the renin-angiotensin system (RAS) is not only found in the circulation, but also in tissues. All components of the ...
... angiotensin (Ang), and specific receptors (ATR). AGT acts as the precursor molecule for Ang peptides—I, II, III, and IV ... renin-angiotensin system) is the part of the endocrine system that plays a prime role in the control of essential hypertension ... Abbreviations: Ang I: angiotensin I; Ang II: angiotensin II; Ang III: angiotensin III; Ang IV: angiotensin IV; ACE: angiotensin ... Angiotensin-converting enzyme (ACE) converts Ang I into angiotensin II (Ang II) which acts on an angiotensin type 1 (AT1) and ...
... "It is not the answers that enlighten, but the questions." - Ionesco ... Discuss the role of the renin-angiotensin-Aldosterone system (RAS) in development of hypertension ... The renin-angiotensin system (RAS) is a major hormonal autocrine/paracrine system that under normal conditions contributes to ...
Angiotensin II (Ang II) is the major octapeptide of the renin-angiotensin system (RAS). For many decades Ang II was mainly ... Zhao Y, Chen X, Cai L, Yang Y, Sui G and Fu S: Angiotensin II/angiotensin II type I receptor (AT1R) signaling promotes MCF-7 ... Shan T, Zhang L, Zhao C, Chen W, Zhang Y and Li G: Angiotensin-(1-7) and angiotensin II induce the transdifferentiation of ... All components of the RAS (angiotensinogen, angiotensin converting enzyme, angiotensin receptors) are expressed in many types ...
Angiotensin II (ANG II) is integral in regulating blood pressure and plays a role in the pathogenesis of hypertension. In ... Angiotensin II-induced skeletal muscle insulin resistance mediated by NF-ĸB activation via NADPH oxidase. Am J Physiol ... Angiotensin II-induced skeletal muscle insulin resistance mediated by NF-B activation via NADPH oxidase. ... Angiotensin II-induced skeletal muscle insulin resistance mediated by NF-B activation via NADPH oxidase. ...
... Our research is also focused on the clarification of the role of angiotensin II and its ... up-regulation of angiotensin II type 2 receptor function) attenuate chemical carcinogen-induced tumorigenesis in the lung ( ... investigation of whether a positive or negative correlation exists between angiotensin II receptor gene polymorphisms and human ...
Endothelin and angiotensin II stimulation of Na+-H+ exchange is impaired in cardiac hypertrophy.. N Ito, Y Kagaya, E O Weinberg ... ET-1, as well as angiotensin II, and phorbol ester, fail to stimulate forward Na+-H+ exchange in adult hypertrophied myocytes. ... Similar effects were observed in the hypertrophied and control myocytes in response to exposure to 10 nM angiotensin II. ET-1 ...
Effects of angiotensin-converting enzyme inhibition and angiotensin II receptor blockers on cardiac angiotensin converting ... Angiotensin II up-regulates angiotensin I-converting enzyme (ACE), but down-regulates ACE2 via the AT1-ERK/p38 MAP kinase ... The antagonists of the renin-angiotensin-aldosterone system (RAAS) have been shown to interfere with angiotensin converting ... Inhibitors of the renin-angiotensin-aldosterone system and CoViD-19-affected patients: A two-faced Janus?. ...
Angiotensin II is a vasoactive peptide and may act as a growth factor in vascular smooth muscle cells. Experimental injury of ... Angiotensin-converting enzyme binding in the neointima was not different from that in the media of the uninjured aorta. Our ... The affinities of the neointimal receptors to angiotensin II or to the AT1 receptor antagonist, losartan, were not different ... We have examined, using quantitative autoradiography, the expression of angiotensin II receptor subtypes AT1 and AT2, and ...
Non-Angiotensin Effects of Angiotensin-Converting Enzyme Inhibitors Wayne Sunman; Wayne Sunman ... angto-oedema, angiotensin II, angiotensin-converting enzyme inhibitors, bradykinin, cough, endothelium-derived relaxing factor, ... Wayne Sunman, Peter S. Sever; Non-Angiotensin Effects of Angiotensin-Converting Enzyme Inhibitors. Clin Sci (Lond) 1 December ...
Angiotensin II Receptor Blockers (ARBs) help lower your blood pressure. Read about the different types of ARBs, how they work, ... Angiotensin II Receptor Blockers (ARBs). Angiotensin II Receptor Blockers (ARBs) help relax your veins and arteries to lower ...
... , Angiotensin Receptor Blockers (ARBs), Blood, Blood Pressure, Cells, Coronavirus Disease ... ACE2 (angiotensin-converting enzyme-2), Asia, Cells, Coronavirus Disease 2019 (COVID-19), Europe, Genetic Mutations, Institutes ... ACE2 (angiotensin-converting enzyme-2), Coronavirus Disease 2019 (COVID-19), JAMA, New England Journal of Medicine, Nose, ... ACE2 (angiotensin-converting enzyme-2), Biotech, Coronavirus Disease (COVID-19) Pandemic At least three different biotech ...
Angiotensin receptor.... *Angiotensin receptor blockers for the treatment of covid-19: pragmatic, adaptive, multicentre, phase ... These effects were reversed by angiotensin receptor blockers.5. Two studies showed that the Angiotensin II type 1 receptor ( ... Objective To determine whether disrupting the renin angiotensin system with angiotensin receptor blockers will improve clinical ... Effect of discontinuing vs continuing angiotensin-converting enzyme inhibitors and angiotensin ii receptor blockers on days ...
Crystal structure of human Angiotensin-1 converting enzyme N-domain in complex with BPPb ... Angiotensin-converting enzyme. A, B. 629. Homo sapiens. Mutation(s): 8 Gene Names: ACE, DCP, DCP1. EC: 3.2.1 (PDB Primary Data ... Angiotensin-converting enzyme (ACE) is a zinc metalloprotease best known for its role in blood pressure regulation. ACE ... Angiotensin-converting enzyme (ACE) is a zinc metalloprotease best known for its role in blood pressure regulation. ACE ...
Angiotensin-Converting Enzyme Inhibitor Dose Optimization and Its Associated Factors at Felege Hiwot Comprehensive Specialized ... 40. Caldeira D, David C, Sampaio C. Tolerability of angiotensin-receptor blockers in patients with intolerance to angiotensin- ... 31. Gotsman I, Rubonivich S, Azaz-Livshits T. Use of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers ... 39. Raebel M. Hyperkalemia associated with use of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers. ...
Angiotensin-converting enzyme I/D and alpha-adducin Gly460Trp polymorphisms: from angiotensin-converting enzyme activity to ... Influence of gender and genetic variability on plasma angiotensin peptides. J Renin Angiotensin Aldosterone Syst. 2006; 7:92-7 ... Gender association of the angiotensin-converting enzyme gene with ischaemic stroke. J Renin Angiotensin Aldosterone Syst. 2011 ... the angiotensin II, type 1 receptor gene. Regarding the angiotensin-converting enzyme insertion/deletion polymorphism, our ...
Regulation of Renal Hemodyamics by Purinergic Receptors in Angiotensin II -Induced Hypertension. Written By ...
Keywords: Epigenetics, DNA methylation, Angiotensin II receptor, Liver fibrosis, Nonalcoholic steatohepatitis Core tip: We ... This is the first study to show that DNA methylation is potentially involved in the regulation of a renin-angiotensin system- ... DNA methylation of angiotensin II receptor gene in nonalcoholic steatohepatitis-related liver fibrosis ... This study demonstrates for the first time that renin-angiotensin system-related gene expression is regulated by DNA ...
Angiotensin-converting enzyme-related carboxypeptidase (ACE2) is a recently identified zinc metalloprotease with ... The Renin-Angiotensin system and SARS-CoV-2 infection: A role for the ACE2 receptor?. Journal of the Renin-Angiotensin- ... Metabolism of angiotensin peptides by angiotensin converting enzyme 2 (ACE2) and analysis of the effect of excess zinc on ACE2 ... Angiotensin-converting enzyme 2 and new insights into the renin-angiotensin system. Biochemical Pharmacology 2008, 75 (4) , 781 ...
Renin-angiotensin-aldosterone system-Operative pathway regulating vascular volume, salt and water retention. ... Angiotensin receptor blockade binding to angiotensin I receptor is thought to prevent negative effects of angiotensin II escape ... Angiotensin I is converted by angiotensin-converting enzyme to angiotensin II, which is a powerful vasoconstrictor. ... Blockade of the renin-angiotensin-aldosterone system (RASS) with angiotensin-converting enzyme inhibition or angiotensin ...
  • In conclusion, angiotensin II was elevated in severe COVID-19 but was markedly influenced by RAS inhibitors and driven by overall RAS activation. (nature.com)
  • There are several types of drugs which includes ACE inhibitors , angiotensin II receptor blockers (ARBs), and renin inhibitors that interrupt different steps in this system to improve blood pressure. (wikipedia.org)
  • There was no evidence of the benefit when comparing angiotensin receptor blockers with angiotensin-converting enzyme inhibitors and with calcium antagonists. (nih.gov)
  • Angiotensin-converting enzyme inhibitors (ACEi) are commonly used for pediatric cardiology patients. (nih.gov)
  • Wrona W, Budka K, Filipiak KJ, Niewada M, Wojtyniak B, Zdrojewski T. Health outcomes and economic consequences of using angiotensin-converting enzyme inhibitors in comparison with angiotensin receptor blockers in the treatment of arterial hypertension in the contemporary Polish setting. (medscape.com)
  • Cardiovascular risk reduction in hypertension: angiotensin-converting enzyme inhibitors, angiotensin receptor blockers. (medscape.com)
  • Angiotensin-Converting Enzyme Inhibitors in Hypertension: To Use or Not to Use? (medscape.com)
  • The story of angiotensin converting enzyme (ACE) inhibitors started approximately 50 years ago, when it was discovered that human plasma incubated with the venom of the Brazilian viper, Bothrops Jararaca , generated a hypotensive compound. (bmj.com)
  • Role of ACE inhibitors in the renin-angiotensin aldosterone system. (bmj.com)
  • Inhibitors of the renin-angiotensin-aldosterone system and CoViD-19-affected patients: A two-faced Janus? (bmj.com)
  • In this respect, while SARS-CoV-2-infected patients of older age with CVD comorbidities show a more severe clinical course and a worse prognosis, it should be adequately underscored that many of these patients in Italy are currently treated with ACE-inhibitors or angiotensin II receptor blockers (ARBs), which are considered the drugs of first choice for hypertension and other CVD conditions (6). (bmj.com)
  • Angiotensin-converting enzyme inhibitors dose optimizations (ACEIs) are essential to boost the treatment outcome in heart failure patients (HF) with reduced ejection fraction. (dovepress.com)
  • Structure-Guided Chemical Optimization of Bicyclic Peptide (Bicycle) Inhibitors of Angiotensin-Converting Enzyme 2. (acs.org)
  • Development of Potent and Selective Phosphinic Peptide Inhibitors of Angiotensin-Converting Enzyme 2. (acs.org)
  • Both ACE inhibitors and ARBs retard the decline in GFR associated with proteinuria which suggests that the renin-angiotensin system plays a significant role in the pathogenesis of chronic renal disease. (standardofcare.com)
  • Prolonged treatment with ACE inhibitors can lead to a partial escape of the renin-angiotensin system (RAS) via the ACE independent generation of angiotensin II by chymase, an enzyme secreted by the heart (Urata H). (standardofcare.com)
  • Since ACE inhibitors do not completely suppress angiotensin II production and its effects, a rationale has been set forth to use ACE inhibitors and ARB in combination for more complete blockade of the renin-angiotensin system. (standardofcare.com)
  • Several studies have assessed the effect of angiotensin converting enzyme inhibitors (ACEIs) on endothelial dysfunction as measured by brachial flow-mediated vasodilatation (FMD). (unboundmedicine.com)
  • Based on initial reports from China, and subsequent evidence that arterial hypertension may be associated with increased risk of mortality in hospitalized COVID-19 infected subjects, hypotheses have been put forward to suggest a potential adverse effects of angiotensin converting enzyme inhibitors (ACE-i) or Angiotensin Receptor Blockers (ARBs). (escardio.org)
  • The binding studies revealed an increased angiotensin receptor binding in the presence of antiotensinase inhibitors. (aspetjournals.org)
  • The effectiveness of angiotensin converting enzyme (ACE) inhibitors in reducing heart failure mortality 1 may be largely attributable to hormone suppression. (bmj.com)
  • ACE inhibitors (angiotensin converting enzyme inhibitors) and ARBs (angiotensin II receptor blockers) work by opening blood vessels and lowering blood pressure. (medlineplus.gov)
  • A new drug class called angiotensin receptor-neprilysin inhibitors (ARNI's) combines an ARB drug with a new type of drug. (medlineplus.gov)
  • Drugs used include diuretics, digoxin, and angiotensin-converting enzyme (ACE) inhibitors. (medscape.com)
  • Some medications (e.g., angiotensin-converting enzyme (ACE) inhibitors) [NHLBI 2007]. (cdc.gov)
  • The brain has shown the presence of various components of brain RAS such as angiotensinogen (AGT), converting enzymes, angiotensin (Ang), and specific receptors (ATR). (hindawi.com)
  • All components of the RAS (angiotensinogen, angiotensin converting enzyme, angiotensin receptors) are expressed in many types of tumours, including endometrial cancer ( 2 , 4 ). (spandidos-publications.com)
  • Moreover, both angiotensin receptors (AT1 and AT2) are overexpressed in different types of cancers, which confirms the role of local RAS in cancer development and progression ( 3 , 5 - 8 ). (spandidos-publications.com)
  • Balloon angioplasty enhances the expression of angiotensin II AT1 receptors in neointima of rat aorta. (jci.org)
  • In contrast to the normal aortic wall, which contained both AT1 and AT2 receptors (80% and 20%, respectively), neointimal cells expressed almost exclusively angiotensin II AT1 receptors. (jci.org)
  • The affinities of the neointimal receptors to angiotensin II or to the AT1 receptor antagonist, losartan, were not different from those in the normal aortic wall. (jci.org)
  • Our data suggest that angiotensin II AT1 receptors may have a significant role in injury-induced vascular smooth muscle proliferation and migration. (jci.org)
  • Angiotensin II binds to angiotensin I receptors and leads to increased blood pressure, sodium retention, heart fibrosis and remodeling, glomerular hypertension, proteinuria and glomerulosclerosis. (standardofcare.com)
  • Angiotensin II can also bind to angiotensin II receptors, which can lead to antifibrotic and anti-inflammatory effects, counteracting effects of angiotensin I binding. (standardofcare.com)
  • Angiotensin II receptors are more prevalent in the fetus and have their role in adults is not defined. (standardofcare.com)
  • Angiotensin receptor blockade binding to angiotensin I receptor is thought to prevent negative effects of angiotensin II escape and promtes binding of angiotensin II to other targets, such as angiotensin II receptors. (standardofcare.com)
  • The increased maximal response and delayed relaxation time observed with caproic acid might be due to uncovering of additional angiotensin receptors and increased agonist availability at the receptor site after angiotensinase blockade. (aspetjournals.org)
  • These data support an important role for both AmA and AmM activities in the metabolism of circulating angiotensins and establish both the value and limitations of amastatin as an inhibitor of peripheral angiotensin metabolism. (aspetjournals.org)
  • How often are angiotensin II and aldosterone concentrations raised during chronic ACE inhibitor treatment in cardiac failure? (bmj.com)
  • OBJECTIVE Angiotensin II (AII) and aldosterone are not always fully suppressed during chronic angiotensin converting enzyme (ACE) inhibitor treatment. (bmj.com)
  • 2 , 3 However, the reductions in angiotensin II (AII) and aldosterone may not be maintained with chronic ACE inhibitor treatment. (bmj.com)
  • Enalapril is a competitive ACE inhibitor that reduces angiotensin II levels and decreases aldosterone secretion. (medscape.com)
  • ACE2 counteracts angiotensin II by converting it to potentially protective angiotensin 1-7. (nature.com)
  • We estimated ACE activity using the angiotensin II:I ratio (ACE-S) and estimated systemic alt-RAS activation using the ratio of alt-RAS axis metabolites to PRA-S (ALT-S). We applied mixed linear models to assess how PRA-S and ACE/ACE2 concentrations affected ALT-S, ACE-S, and angiotensins II and 1-7. (nature.com)
  • ACE2 also predicted angiotensin 1-7 levels and ALT-S. No single factor or the combined model, however, could fully explain ACE-S. ACE2 and ACE-S trajectories in severe COVID-19 did not differ between survivors and non-survivors. (nature.com)
  • A shift to the alt-RAS axis because of increased ACE2 could partially explain the relative reduction in angiotensin II levels. (nature.com)
  • Angiotensin-converting enzyme-related carboxypeptidase (ACE2) is a recently identified zinc metalloprotease with carboxypeptidase activity that was identified using our genomics platform. (acs.org)
  • We characterized the pathological findings in 72 mink from US farm s with SARS-CoV-2 outbreaks, localized SARS-CoV-2 and its host cellular receptor angiotensin-converting enzyme 2 (ACE2) in mink respiratory tissues, and evaluated the utility of various test methods and specimens for SARS-CoV-2 detection in necropsy tissues. (cdc.gov)
  • They identified a new association with a rare genetic variant at the Xp22.2 locus (rs190509934) that downregulates the expression of angiotensin-converting enzyme 2 (ACE2). (cdc.gov)
  • Angiotensinogen is an α-2-globulin synthesized in the liver and is a precursor for angiotensin, but has also been indicated as having many other roles not related to angiotensin peptides. (wikipedia.org)
  • Plasma angiotensinogen levels are increased by plasma corticosteroid, estrogen, thyroid hormone, and angiotensin II levels. (wikipedia.org)
  • Angiotensin I (CAS# 11128-99-7), officially called proangiotensin, is formed by the action of renin on angiotensinogen. (wikipedia.org)
  • Plasma renin then carries out the conversion of angiotensinogen , released by the liver , to a decapeptide called angiotensin I . [4] Angiotensin I is subsequently converted to angiotensin II (an octapeptide) by the angiotensin-converting enzyme (ACE) found on the surface of vascular endothelial cells, predominantly those of the lungs . (wikipedia.org)
  • Conventional RAS involves the conversion of inactive angiotensinogen into angiotensin I (Ang I) in the presence of renin which is released from the kidney in response to low blood volume. (hindawi.com)
  • Intrinsic brain RAS is an enzyme-neuropeptide system having functional components (angiotensinogen, peptidases, angiotensin, and specific receptor proteins) with important biological and neurobiological activities in the brain. (hindawi.com)
  • We examined the association of the insertion/deletion (I/D) polymorphism of the angiotensin-converting enzyme gene, of the M235T polymorphism of the angiotensinogen gene, and of the A1166C polymorphism of the angiotensin II type 1 receptor gene with NAION. (molvis.org)
  • NAION occurrence was not associated with the M235T polymorphism of the angiotensinogen gene and the A1166C polymorphism of the angiotensin II, type 1 receptor gene. (molvis.org)
  • The renin-angiotensin system genes exhibit three common polymorphisms: the insertion/deletion (I/D) polymorphism of the angiotensin-converting enzyme ( ACE ) gene, the M235T polymorphism of the angiotensinogen gene ( AGT ), and the A1166C polymorphism of the angiotensin II type 1 receptor gene ( AT1-receptor ). (molvis.org)
  • Renin then enters the blood where it catalyzes a protein called angiotensinogen to angiotensin I. (standardofcare.com)
  • The liver secretes inactive angiotensinogen, which is converted by renally secreted renin to angiotensin I. (standardofcare.com)
  • Angiotensinogen is encoded by the gene AGT, and is a glycoprotein secreted by hepatocytes that is cleaved by renin to yield angiotensin I which is further cleave to generate angiotensin II. (standardofcare.com)
  • Angiotensinogen is the rate limiting factor in the production of angiotensinII, and evidence links angiotensinogen and angiotensin II to hypertension: the greater the copy number of angiotensin heme, the higher the blood pressure. (standardofcare.com)
  • Renin catalyzes inactive angiotensinogen to angiotensin I. (standardofcare.com)
  • Renin cleaves angiotensinogen to angiotensin I, which is in turn converted by angiotensin-converting enzyme (ACE) to angiotensin II. (standardofcare.com)
  • Angiotensin II Receptor Blockers (ARBs) help relax your veins and arteries to lower your blood pressure, making it easier for your heart to pump. (heartfoundation.org.nz)
  • MEDLINE, EMBASE and Cochrane Central Register of Controlled Trials (CENTRAL) were searched from 1996 to October 2010 on randomised controlled trials (RCTs) that assessed the effect of ACEIs on brachial FMD versus placebo or no treatment and ACEIs versus angiotensin receptor blockers (ARBs), calcium channel blockers (CCBs) and β-blockers. (unboundmedicine.com)
  • The aim of this meta-analysis was to investigate the effects of angiotensin receptor blockers on the risk of stroke. (nih.gov)
  • The observation was then made by Vane that these peptides could also block the conversion of angiotensin I into angiotensin II via the angiotensin converting enzyme. (bmj.com)
  • Captopril prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in increased levels of plasma renin and a reduction in aldosterone secretion. (medscape.com)
  • Lisinopril prevents conversion of angiotensin I to angiotensin II, resulting in decreased aldosterone secretion. (medscape.com)
  • Alchemedicine Inc. has prepared and tested new angiotensin AT1 receptor (AGTR1) antagonists reported to be useful for the treatment of cancer, hypertension, glaucoma and renal disorders. (bioworld.com)
  • The RAS (renin-angiotensin system) is the part of the endocrine system that plays a prime role in the control of essential hypertension. (hindawi.com)
  • Angiotensin II (ANG II) is integral in regulating blood pressure and plays a role in the pathogenesis of hypertension. (biosyn.com)
  • Several single nucleotide polymorphisms (SNPs) of renin-angiotensin system (RAS) genes are associated with hypertension (HT) but most of them are focusing on single locus effects. (hindawi.com)
  • Objective To determine whether disrupting the renin angiotensin system with angiotensin receptor blockers will improve clinical outcomes in people with covid-19. (bmj.com)
  • Regarding the angiotensin-converting enzyme insertion/deletion polymorphism, our findings suggest that the II genotype could be a risk factor for NAION in younger male patients when compared to all cases and controls (p=0.033, odds ratio=5.71, confidence interval=1.152¨C28.35 and p=0.03, odds ratio=5.33, confidence interval=1.17¨C24.31 respectively). (molvis.org)
  • The D allele of angiotensin I-converting enzyme gene insertion/deletion polymorphism is associated with the severity of atherosclerosis" Clinical Chemistry and Laboratory Medicine , vol. 46, no. 4, 2008, pp. 446-452. (degruyter.com)
  • Niemiec, P., Zak, I. and Wita, K. (2008) The D allele of angiotensin I-converting enzyme gene insertion/deletion polymorphism is associated with the severity of atherosclerosis. (degruyter.com)
  • The renin-angiotensin system ( RAS ), or renin-angiotensin-aldosterone system ( RAAS ), is a hormone system that regulates blood pressure , fluid and electrolyte balance, and systemic vascular resistance . (wikipedia.org)
  • The antagonists of the renin-angiotensin-aldosterone system (RAAS) have been shown to interfere with angiotensin converting enzyme (ACE)-2 receptor expression in heart and kidney tissues. (bmj.com)
  • Forty-seven patients with NAION and 76 controls, age- and gender-matched, were recruited and genotyped for renin-angiotensin-aldosterone system (RAAS) genes. (molvis.org)
  • Autosomal recessively inherited pathogenic variants in genes associated with the renin-angiotensin-aldosterone system (RAAS) result in early onset oligohydramnios and clinical features of the Potter sequence, typically in association with proximal renal tubules dysgenesis. (bepress.com)
  • SARS-CoV-2 gains cell entry via angiotensin-converting enzyme (ACE) 2, a membrane-bound enzyme of the "alternative" (alt) renin-angiotensin system (RAS). (nature.com)
  • Angiotensin I is then converted to an octapeptide , angiotensin II by angiotensin-converting enzyme (ACE), [9] which is thought to be found mainly in endothelial cells of the capillaries throughout the body, within the lungs and the epithelial cells of the kidneys. (wikipedia.org)
  • Angiotensin-converting enzyme (ACE) converts Ang I into angiotensin II (Ang II) which acts on an angiotensin type 1 (AT1) and angiotensin type 2 (AT2) receptor. (hindawi.com)
  • We have examined, using quantitative autoradiography, the expression of angiotensin II receptor subtypes AT1 and AT2, and angiotensin-converting enzyme, in the neointima formed in the rat thoracic aorta 15 d after balloon-catheter injury. (jci.org)
  • Angiotensin-converting enzyme binding in the neointima was not different from that in the media of the uninjured aorta. (jci.org)
  • Angiotensin-converting enzyme (ACE) is a zinc metalloprotease best known for its role in blood pressure regulation. (rcsb.org)
  • Angiotensin-Converting Enzyme 2 Ectodomain Shedding Cleavage-Site Identification: Determinants and Constraints. (acs.org)
  • Angiotensin I is converted by angiotensin-converting enzyme to angiotensin II, which is a powerful vasoconstrictor. (standardofcare.com)
  • Blockade of the renin-angiotensin-aldosterone system (RASS) with angiotensin-converting enzyme inhibition or angiotensin receptor blockade are central therapies for both renal and cardiovascular protection in patients with chronic kidney disease. (standardofcare.com)
  • Angiotensin I Converting Enzyme 2 (ACE-2) Inhib. (anaspec.com)
  • Sex differences in angiotensin-converting enzyme modulation of Ang (1-7) levels in normotensive WKY rats. (anaspec.com)
  • The study aims to examine the effects of coenzyme Q10, (a bioenergetic antioxidant), on the indexes of left ventricular remodeling, oxidative damage, and angiotensin-converting enzyme (ACE) level after acute myocardial infarction (AMI) with left ventricular dysfunction. (mdpi.com)
  • Angiotensin-converting enzyme (ACE) is crucial in the synthesis of angiotensin II, breakdown of bradykinin and the hydrolysis of several other neuropeptides such as enkephalin, substance P, dynorphin and neurotensin. (unboundmedicine.com)
  • Angiotensin II is produced primarily by angiotensin I-converting enzyme (ACE) within atherosclerotic lesions and ACE level in plaques correlates with the severity of vessel wall damage. (degruyter.com)
  • To our knowledge, angiotensin converting enzyme ( ACE ) gene I/D polymorphisms have not yet been investigated in AS patients in Turkish population.This study was conducted in Turkish patients with AS to determine the frequency of I/D polymorphism genotypes of angiotensin converting enzyme gene. (molvis.org)
  • As a result of our study, angiotensin converting enzyme gene I/D polymorphism DD genotype could be a genetic marker in ankylosing spondylitis in a Turkish study population. (molvis.org)
  • We aimed to identify the relationship between adiposity and blood pressure, independent of a robust set of lifestyle and metabolic factors, and to examine the modulating role of sex and Angiotensin-Converting Enzyme (ACE) insertion/deletion (I/D) polymorphisms. (lu.se)
  • Compared with Sprague-Dawley normtensive control rats, Ren-2 skeletal muscle exhibited significantly increased oxidative stress, NF-ĸB activation, and TNF-α expression, which were attenuated by in vivo treatment with an angiotensin type 1 receptor blocker (valsartan) or SOD/catalase mimetic (tempol). (biosyn.com)
  • angiotensin II type 1 receptor, AT 1 R ) in HT and non-HT subjects were included that showed no significant genotype differences. (hindawi.com)
  • Angiotensin is a peptide hormone that causes vasoconstriction and an increase in blood pressure. (wikipedia.org)
  • Angiotensin II is a potent vasoconstrictive peptide that causes blood vessels to narrow, resulting in increased blood pressure. (wikipedia.org)
  • Angiotensin II is a vasoactive peptide and may act as a growth factor in vascular smooth muscle cells. (jci.org)
  • Throughout the body, angiotensin II is a potent vasoconstrictor of arterioles . (wikipedia.org)
  • Dihydropyridine calcium channel blockers, such as amlodipine, and angiotensin receptor blockers, such as valsartan, represent the two antihypertensive drug classes with the strongest supportive data for the prevention of stroke. (dovepress.com)
  • Importantly, alternative pathways exist such as the kinase pathway, which bypass ACE in the generation of angiotensin II. (bmj.com)
  • In heart failure decreased cardiac output and reduced renal perfusion leads to stimulation of plasma renin activity and thus to release of angiotensin II and aldosterone. (standardofcare.com)
  • 1. To examine the response of renal prostaglandins (PG) to systemic and renal vasoconstriction noradrenaline (NA), arginine vasopressin (AVP) and angiotensin II (ANG II) were each infused into eight healthy female subjects for 3 h on different days. (portlandpress.com)
  • Therefore, various biologically active peptides such as angiotensin, affecting cell proliferation, have become a new area of study in endometrial cancer research. (spandidos-publications.com)
  • Angiotensin also stimulates the release of aldosterone from the adrenal cortex to promote sodium retention by the kidneys. (wikipedia.org)
  • [6] Angiotensin II also stimulates the secretion of the hormone aldosterone [6] from the adrenal cortex . (wikipedia.org)
  • Angiotensin II also stimulates the production of aldosterone from the adrenal cortex, which causes the tubules of the kidneys to increase reabsorption of sodium, with water following, thereby increasing plasma volume, and thus also blood pressure. (standardofcare.com)
  • Angiotensin II reaches the posterior pituitary gland and the adrenal cortex, where it causes a cascade effect of hormones that cause the kidneys to retain water and sodium, increasing blood pressure. (standardofcare.com)
  • Angiotensin 1-7 acts via an 'alternative' RAS pathway. (nature.com)
  • The renin-angiotensin system (RAS) is of paramount importance, having a role in the regulatory pathway involved in the maintenance of blood pressure (BP), body fluid volume, and sodium homeostasis. (hindawi.com)
  • Despite initial fears , evidence from retrospective observational studies supports the inhibition of the renin-angiotensin system as an emerging pathway to delay or moderate angiotensin II -driven lung inflammation . (bvsalud.org)
  • The experiment assesses whether test articles cause vasoconstriction in human subcutaneous resistance arteries with PDA-angiotensin 1 as a reference compound. (reprocell.com)
  • Angiotensin was isolated in the late 1930s (first named 'angiotonin' or 'hypertensin') and subsequently characterized and synthesized by groups at the Cleveland Clinic and Ciba laboratories. (wikipedia.org)
  • Angiotensin was discovered during the late 1930s concurrently by Page in the United States and by Braun-Menenez and his colleagues in South America [ 2 ]. (hindawi.com)
  • Angiotensin receptor blockers are widely used in patients at high risk of cardiocerebrovascular events. (nih.gov)
  • Chez les patients hypertendus, le taux de mortalité était plus élevé uniquement chez les patients admis pour un infarctus du myocarde avec sus-décalage du segment ST. Après ajustement des résultats en fonction des variables de référence, l'hypertension s'est révélé être un facteur prédictif indépendant de l'insuffisance cardiaque (OR = 1,31) et de l'accident vasculaire cérébral (OR = 2,47). (who.int)
  • Progressive activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system contributes to chronic heart failure, including that which occurs after acute myocardial infarction. (standardofcare.com)
  • The role of the sympathetic nervous system, epinephrine, norepinephrine, adrenocorticotrophic hormone, and the renin angiotensin aldosterone system in the control of blood pressure was discussed. (cdc.gov)
  • An oligopeptide, angiotensin is a hormone and a dipsogen. (wikipedia.org)
  • The renin-angiotensin system (RAS) is a complex network that regulates blood pressure and blood volume through the hormone angiotensin II via its type 1 (AT 1 ) receptor ('classical' RAS) 1 . (nature.com)
  • Angiotensin II acts as an endocrine , autocrine / paracrine , and intracrine hormone. (wikipedia.org)
  • The signaling pathways linking angiotensin II to CTGF formation are, however, incompletely understood. (amrita.edu)
  • It is part of the renin-angiotensin system, which regulates blood pressure. (wikipedia.org)
  • One is in the synthesis of angiotensin II, which has vasoconstrictive properties, promotes retention of sodium and water, and promotes cell growth. (bmj.com)
  • Angiotensin II levels are not completely suppressed with ACE inhibition, a process known as angiotensin II escape. (standardofcare.com)
  • Consistent with the lower inhibition of AmA, the potency of angiotensin I and AII were only slightly increased after amastatin. (aspetjournals.org)
  • Ionesco The renin-angiotensin system (RAS) is a major hormonal autocrine/paracrine system that under normal conditions contributes to the regulation of. (cyberounds.com)
  • The present study explored whether SGK1 is transcriptionally regulated by angiotensin II and participates in the angiotensin II-dependent regulation of CTGF expression. (amrita.edu)
  • Role of aminopeptidase activity in the regulation of the pressor activity of circulating angiotensins. (aspetjournals.org)
  • Angiotensin Receptor Blockers for COVID-19: Pathophysiological and Pharmacological Considerations About Ongoing and Future Prospective Clinical Trials. (bvsalud.org)
  • In this commentary we provide an overview and analysis of current ongoing clinical trials aimed at evaluating the therapeutic efficacy of angiotensin receptor blocker (ARB) use in COVID-19. (bvsalud.org)
  • Caproic acid significantly increased the maximal response to angiotensin and delayed the relaxation time of contracted aortic strips. (aspetjournals.org)
  • In the kidneys, angiotensin II constricts glomerular arterioles, having a greater effect on efferent arterioles than afferent. (wikipedia.org)
  • Angiotensin II has both direct and indirect effects on blood pressure. (standardofcare.com)
  • The renin-angiotensin system (RAS) represents a critical endocrine regulator for maintaining blood pressure and blood fluid volume in the circulatory system. (hindawi.com)
  • In order to examine metabolism in vivo, blood pressure responses to angiotensins were obtained in anesthesized rats before and during infusion of amastatin (16 nmol/min i.v.). Amastatin specifically inhibited plasma AmM and AmA activities 81 and 10%, respectively. (aspetjournals.org)
  • However, the potency of AIII and des(Asp1)angiotensin I were significantly increased regarding both maximal change in blood pressure and duration of action. (aspetjournals.org)
  • To do this, angiotensin II constricts efferent arterioles, which forces blood to build up in the glomerulus, increasing glomerular pressure. (wikipedia.org)
  • Then, it is rapidly degraded into a heptapeptide called angiotensin III by angiotensinases which are present in red blood cells and vascular beds in many tissues. (wikipedia.org)
  • Also, the renin-angiotensin system (RAS) is not only found in the circulation, but also in tissues. (bmj.com)