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%).
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 ZINC-dependent membrane-bound aminopeptidase that catalyzes the N-terminal peptide cleavage of GLUTAMATE (and to a lesser extent ASPARTATE). The enzyme appears to play a role in the catabolic pathway of the RENIN-ANGIOTENSIN SYSTEM.
Cell surface proteins that bind ANGIOTENSINS and trigger intracellular changes influencing the behavior of cells.
An angiotensin receptor subtype that is expressed at high levels in a variety of adult tissues including the CARDIOVASCULAR SYSTEM, the KIDNEY, the ENDOCRINE SYSTEM and the NERVOUS SYSTEM. Activation of the type 1 angiotensin receptor causes VASOCONSTRICTION and sodium retention.
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 angiotensin receptor subtype that is expressed at high levels in fetal tissues. Many effects of the angiotensin type 2 receptor such as VASODILATION and sodium loss are the opposite of that of the ANGIOTENSIN TYPE 1 RECEPTOR.
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.
Zinc-binding metalloproteases that are members of the type II integral membrane metalloproteases. They are expressed by GRANULOCYTES; MONOCYTES; and their precursors as well as by various non-hematopoietic cells. They release an N-terminal amino acid from a peptide, amide or arylamide.
Agents that antagonize ANGIOTENSIN RECEPTORS. Many drugs in this class specifically target the ANGIOTENSIN TYPE 1 RECEPTOR.
Agents that antagonize ANGIOTENSIN II TYPE 1 RECEPTOR. Included are ANGIOTENSIN II analogs such as SARALASIN and biphenylimidazoles such as LOSARTAN. Some are used as ANTIHYPERTENSIVE AGENTS.
Agents that antagonize the ANGIOTENSIN II TYPE 2 RECEPTOR.
Endogenous or exogenous chemicals that regulate the WATER-ELECTROLYTE BALANCE in the body. They consist of peptides and non-peptide compounds.
The octapeptide amide of bovine angiotensin II used to increase blood pressure by vasoconstriction.
An octapeptide analog of angiotensin II (bovine) with amino acids 1 and 8 replaced with sarcosine and alanine, respectively. It is a highly specific competitive inhibitor of angiotensin II that is used in the diagnosis of HYPERTENSION.
Inorganic compounds that contain gold as an integral part of the molecule.
Tetrazoles are heterocyclic organic compounds containing a 1,3,5-triazole ring with an additional nitrogen atom, often used in pharmaceuticals as bioisosteres for carboxylic acid groups due to their isoelectronic nature and similar hydrogen bonding capabilities.
An antagonist of ANGIOTENSIN TYPE 1 RECEPTOR with antihypertensive activity due to the reduced pressor effect of ANGIOTENSIN II.
Inorganic or organic oxy acids of sulfur which contain the RSO2(OH) radical.
A subclass of EXOPEPTIDASES that act on the free N terminus end of a polypeptide liberating a single amino acid residue. EC 3.4.11.
Compounds with a BENZENE fused to IMIDAZOLES.
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.
Compounds containing 1,3-diazole, a five membered aromatic ring containing two nitrogen atoms separated by one of the carbons. Chemically reduced ones include IMIDAZOLINES and IMIDAZOLIDINES. Distinguish from 1,2-diazole (PYRAZOLES).
Sodium excretion by URINATION.
PRESSURE of the BLOOD on the ARTERIES and other BLOOD VESSELS.
Compounds with a six membered aromatic ring containing NITROGEN. The saturated version is PIPERIDINES.
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 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 strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.
An ANGIOTENSIN II analog which acts as a highly specific inhibitor of ANGIOTENSIN TYPE 1 RECEPTOR.
Biphenyl compounds are organic substances consisting of two phenyl rings connected by a single covalent bond, and can exhibit various properties and uses, including as intermediates in chemical synthesis, components in plastics and dyes, and as additives in fuels.
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.
Drugs used to cause constriction of the blood vessels.
A sulfur-containing essential L-amino acid that is important in many body functions.
Hypertension due to RENAL ARTERY OBSTRUCTION or compression.
Narrowing or occlusion of the RENAL ARTERY or arteries. It is due usually to ATHEROSCLEROSIS; FIBROMUSCULAR DYSPLASIA; THROMBOSIS; EMBOLISM, or external pressure. The reduced renal perfusion can lead to renovascular hypertension (HYPERTENSION, RENOVASCULAR).
A branch of the abdominal aorta which supplies the kidneys, adrenal glands and ureters.
Pathological processes which result in the partial or complete obstruction of ARTERIES. They are characterized by greatly reduced or absence of blood flow through these vessels. They are also known as arterial insufficiency.
Persistent high BLOOD PRESSURE due to KIDNEY DISEASES, such as those involving the renal parenchyma, the renal vasculature, or tumors that secrete RENIN.
Persistently high systemic arterial BLOOD PRESSURE. Based on multiple readings (BLOOD PRESSURE DETERMINATION), hypertension is currently defined as when SYSTOLIC PRESSURE is consistently greater than 140 mm Hg or when DIASTOLIC PRESSURE is consistently 90 mm Hg or more.

Angiotensin receptor subtype 1 mediates angiotensin II enhancement of isoproterenol-induced cyclic AMP production in preglomerular microvascular smooth muscle cells. (1/90)

In a previous study, we found that angiotensin (Ang) II enhances beta-adrenoceptor-induced cAMP production in cultured preglomerular microvascular smooth muscle cells (PMVSMCs) obtained from spontaneously hypertensive rats. The purpose of the present investigation was to identify the Ang receptor subtypes that mediate this effect. In our first study, we compared the ability of Ang II, Ang III, Ang (3-8), and Ang (1-7) to increase cAMP production in isoproterenol (1 microM)-treated PMVSMCs. Each peptide was tested at 0.1, 1, 10, 100, and 1000 nM. Both Ang II and Ang III increased intracellular (EC50s, 1 and 11 nM, respectively) and extracellular (EC50s, 2 and 14 nM, respectively) cAMP levels in a concentration-dependent fashion. In contrast, Ang (3-8) and Ang (1-7) did not enhance either intracellular or extracellular cAMP levels at any concentration tested. In our second study, we examined the ability of L 158809 [a selective Ang receptor subtype 1 (AT1) receptor antagonist] to inhibit Ang II (100 nM) and Ang III (100 nM) enhancement of isoproterenol (1 microM)-induced cAMP production in PMVSMCs. L 158809 (10 nM) abolished or nearly abolished (p <.001) Ang II and Ang III enhancement of isoproterenol-induced intracellular and extracellular cAMP levels. In contrast, PD 123319 (300 nM; a selective AT2 receptor antagonist) did not significantly alter Ang II enhancement of isoproterenol-induced intracellular or extracellular cAMP levels. We conclude that AT1 receptors, but not AT2, Ang (3-8), nor Ang (1-7) receptors mediate Ang II and Ang III enhancement of beta-adrenoceptor-induced cAMP production in cultured PMVSMCs.  (+info)

Prejunctional angiotensin receptors involved in the facilitation of noradrenaline release in mouse tissues. (2/90)

The effect of angiotensin II, angiotensin III, angiotensin IV and angiotensin-(1-7) on the electrically induced release of noradrenaline was studied in preparations of mouse atria, spleen, hippocampus, occipito-parietal cortex and hypothalamus preincubated with [3H]-noradrenaline. The prejunctional angiotensin receptor type was investigated using the non-selective receptor antagonist saralasin (AT1/AT2) and the AT1 and AT2 selective receptor antagonists losartan and PD 123319, respectively. In atrial and splenic preparations, angiotensin II (0.01 nM-0.1 microM) and angiotensin III (0.01 and 0.1 nM-1 microM) increased the stimulation-induced overflow of tritium in a concentration-dependent manner. Angiotensin IV, only at high concentrations (1 and 10 pM), enhanced tritium overflow in the atria, while angiotensin-(1-7) (0.1 nM-10 microM) was without effect in both preparations. In preparations of hippocampus, occipito-parietal cortex and hypothalamus, none of the angiotensin peptides altered the evoked overflow of tritium. In atrial and splenic preparations, saralasin (0.1 microM) and losartan (0.1 and 1 microM), but not PD 123319 (0.1 microM), shifted the concentration-response curves of angiotensin II and angiotensin III to the right. In conclusion, in mouse atria and spleen, angiotensin II and angiotensin III facilitate the action potential induced release of noradrenaline via a prejunctional AT1 receptor. Only high concentrations of angiotensin IV are effective in the atria and angiotensin-(1-7) is without effect in both preparations. In mouse brain areas, angiotensin II, angiotensin III, angiotensin IV and angiotensin-(1-7) do not modulate the release of noradrenaline.  (+info)

Aminopeptidase A activity and angiotensin III effects on [Ca2+]i along the rat nephron. (3/90)

BACKGROUND: This study examined the specific effects of angiotensin III (Ang III) along the nephron. METHODS: We examined the distribution of aminopeptidase A (APA) activity by using a specific APA inhibitor and by immunostaining with an antirat kidney APA antibody, the Ang III-induced variations of [Ca2+]i by using fura-2 and the characterization of the receptor subtype involved in the response to Ang III in cortical thick ascending limb (CTAL). RESULTS: APA activity was found all along the nephron but was higher in the cortex than in the medulla. This was confirmed by immunostaining. Increases in [Ca2+]i elicited by 10(-7) mol/liter Ang III were observed all along the nephron. The characterization of the receptor subtype involved in the [Ca2+]i response to Ang III in CTAL indicated that EC50 values for Ang III and Ang II were similar (13.5 and 10.3 nmol/liter, respectively), and Ang III-induced responses were totally abolished by AT1 receptor but not by AT2 receptor antagonists. There was a cross-desensitization of [Ca2+]i responses to 10(-7) mol/liter Ang III and Ang II, and the [Ca2+]i responses to 10(-7) mol/liter Ang II and Ang III were not additive. CONCLUSION: These results show that in CTAL, the [Ca2+]i responses to Ang II and Ang III occur through the same AT1a receptor because this subtype is predominant in this segment. Taken together, these data suggest that APA could be a key enzyme to generate Ang III from Ang II in the kidney.  (+info)

Aminopeptidase A inhibitors as potential central antihypertensive agents. (4/90)

Overactivity of the brain renin-angiotensin system (RAS) has been implicated in the development and maintenance of hypertension in several experimental models, such as spontaneously hypertensive rats and transgenic mice expressing both human renin and human angiotensinogen transgenes. We recently reported that, in the murine brain, angiotensin II (AngII) is converted to angiotensin III (AngIII) by aminopeptidase A (APA), whereas AngIII is inactivated by aminopeptidase N (APN). If injected into cerebral ventricles (ICV), AngII and AngIII cause similar pressor responses. Because AngII is metabolized in vivo into AngIII, the exact nature of the active peptide is not precisely determined. Here we report that, in rats, ICV injection of the selective APA inhibitor EC33 [(S)-3-amino-4-mercaptobutyl sulfonic acid] blocked the pressor response of exogenous AngII, suggesting that the conversion of AngII to AngIII is required to increase blood pressure (BP). Furthermore, ICV injection, but not i.v. injection, of EC33 alone caused a dose-dependent decrease in BP by blocking the formation of brain but not systemic AngIII. This is corroborated by the fact that the selective APN inhibitor, PC18 (2-amino-4-methylsulfonyl butane thiol), administered alone via the ICV route, increases BP. This pressor response was blocked by prior treatment with the angiotensin type 1 (AT(1)) receptor antagonist, losartan, showing that blocking the action of APN on AngIII metabolism leads to an increase in endogenous AngIII levels, resulting in BP increase, through interaction with AT(1) receptors. These data demonstrate that AngIII is a major effector peptide of the brain RAS, exerting tonic stimulatory control over BP. Thus, APA, the enzyme responsible for the formation of brain AngIII, represents a potential central therapeutic target that justifies the development of APA inhibitors as central antihypertensive agents.  (+info)

Primary and secondary locations of charge sites in angiotensin II (M + 2H)2+ ions formed by electrospray ionization. (5/90)

High-energy tandem mass spectrometry and molecular dynamics calculations are used to determine the locations of charge in metastably decomposing (M + 2H)2+ ions of human angiotensin II. Charge-separation reactions provide critical information regarding charge sites in multiple charged ions. The most probable kinetic energy released (Tm.p.) from these decompositions are obtained using kinetic energy release distributions (KERDs) in conjunction with MS/MS (MS2), MS/MS/MS (MS3), and MS/MS/MS/MS (MS4) experiments. The most abundant singly and doubly charged product ions arise from precursor ion structures in which one proton is located on the arginine (Arg) side chain and the other proton is located on a distal peptide backbone carbonyl oxygen. The MS3 KERD experiments show unequivocally that neither the N-terminal amine nor the aspartic acid (Asp) side chain are sites of protonation. In the gas phase, protonation of the less basic peptide backbone instead of the more proximal and basic histidine (His) side chain is favored as a result of reduced coulomb repulsion between the two charge sites. The singly and doubly charged product ions of lesser abundance arise from precursor ion structures in which one proton is located on the Arg side chain and the other on the His side chain. This is demonstrated in the MS3 and MS4 mass-analyzed ion kinetic energy spectrometry experiments. Interestingly, (b7" + OH)2+ product ions, like the (M + 2H)2+ ions of angiotensin II, are observed to have at least two different decomposing structures in which charge sites have a primary and secondary location.  (+info)

Angiotensin III depressor action in the conscious rabbit is blocked by losartan but not PD 123319. (6/90)

Vasodilator and vasodepressor properties of angiotensins have been reported, and mediation by prostaglandins or nitric oxide has been proposed. Other studies indicate that angiotensin AT(2) receptors might mediate a depressor action, and the present study was designed to delineate and explore this possibility in a conscious rabbit model. Large intravenous boluses of angiotensin III (15 nmol/kg) produced a predictable pressor peak (82+/-4 mm Hg) followed by a depressor phase (20+/-3 mm Hg), whereas equipressor doses of angiotensin II were less effective at producing depressor responses. Angiotensin-(1-7) did not exert a depressor action, and the reduced potency of angiotensin IV (relative to angiotensin III) was similar for both the pressor and depressor phases ( approximately 100-fold). It is clear that specific angiotensin IV or angiotensin-(1-7) receptors do not mediate depressor effects in this model. The AT(1) antagonist losartan (1 mg/kg) blocked both the pressor and depressor components of the angiotensin III response, whereas the AT(2) antagonist PD 123319 (35 mg/kg) had no effect on either element of the response. The data obtained with the angiotensin receptor subtype-selective compounds, losartan and PD 123319, suggest that the depressor action is an AT(1)-mediated effect and give no indication that AT(2) receptors could be involved. Paradoxically, the greater potency of angiotensin III as a vasodepressor belies the conclusion that the response is AT(1)-mediated, because AT(1) receptors have a greater affinity for angiotensin II versus angiotensin III.  (+info)

Enhancement of noradrenaline release by angiotensin II and bradykinin in mouse atria: evidence for cross-talk between G(q/11) protein- and G(i/o) protein-coupled receptors. (7/90)

1. The interaction between alpha(2)-autoreceptors and receptors for angiotensin (AT(1)) and bradykinin (B(2)) was studied in mouse isolated atria. The preparations were labelled with [(3)H]-noradrenaline and then superfused with desipramine-containing medium and stimulated electrically. 2. Angiotensin II (10(-11) - 10(-7) M), angiotensin III (10(-10) - 10(-6) M) and bradykinin (10(-11) - 10(-7) M) enhanced the evoked overflow of tritium when preparations were stimulated with conditions that led to marked alpha(2)-autoinhibition (120 pulses at 3 Hz), but not when stimulated with conditions that led to little alpha(2)-autoinhibition (20 pulses at 50 Hz). 3. Blockade of alpha-adrenoceptors by phentolamine (1 or 10 microM) reduced or abolished the effect of angiotensin II and bradykinin on the overflow response to 120 pulses at 3 Hz. 4. Addition of the delta-opioid agonist [D-Ser(2)]-leucine enkephalin-Thr (DSLET, 0.1 microM), or of neuropeptide Y (0.1 microM), together with phentolamine, restored the effect of angiotensin II and bradykinin. 5. The beta-adrenoceptor agonist terbutaline (10(-9) - 10(-4) M) enhanced the evoked overflow of tritium irrespective of the degree of autoinhibition. 6. The experiments show that (i) a marked prejunctional facilitatory effect of angiotensin and bradykinin in mouse isolated atria requires prejunctional alpha(2)-autoinhibition; (ii) in the absence of alpha(2)-autoinhibition, activation of other prejunctional G(i/o) protein-coupled receptors, namely opioid and neuropeptide Y receptors, restores a marked effect of angiotensin II and bradykinin; and (iii) the facilitatory effect of terbutaline is not dependent upon the degree of alpha(2)-autoinhibition. The findings indicate that the major part of the release-enhancing effect elicited through prejunctional G(q/11) protein-coupled receptors is due to disruption of an ongoing, alpha(2)-autoreceptor-triggered G(i/o) protein mediated inhibition.  (+info)

Angiotensin III increases MCP-1 and activates NF-kappaB and AP-1 in cultured mesangial and mononuclear cells. (8/90)

BACKGROUND: Monocyte infiltration is a common feature of renal diseases. Angiotensin II (Ang II) participates in inflammatory cell infiltration in the kidney. However, the influence of other peptides of the renin-angiotensin system, such as the N-terminal Ang II degradation product Ang III, has not been addressed. METHODS: In cultured renal and mononuclear cells, we investigated whether Ang III is involved in monocyte recruitment through the regulation of the chemokine, monocyte chemoattractant protein-1 (MCP-1; Northern blot, Western blot, immunofluorescence, and chemotaxis), and the activation of transcription factors, nuclear factor kappaB (NF-kappaB) and activating protein-1 (AP-1; electrophoretic mobility shift assay). RESULTS: In cultured rat mesangial and mononuclear cells, Ang III increased MCP-1 gene expression and protein levels. Supernatants from Ang III-treated mesangial cells showed increased chemoattractant activity for monocytes, which was partially inhibited by the addition of anti-MCP-1 antibody. Ang III elicited a rapid NF-kappaB activation (8-fold, after 30 min), showing a kinetics and intensity similar to that observed with Ang II and tumor necrosis factor-alpha. The maximal NF-kappaB activation was correlated with nuclear translocation of p50 and p65 subunits and disappearance of cytosolic IkappaB. Ang III also activated AP-1 (5-fold, after 18 h), while SP-1 was unchanged. Two NF-kappaB inhibitors abolished the Ang III-induced MCP-1 mRNA expression, suggesting that overexpression of this chemokine is mediated, at least in part, by NF-kappaB activation. CONCLUSIONS: Ang III activates the transcription factors NF-kappaB and AP-1 and increases the expression of related genes, such as MCP-1. Our study describes a novel and potent proinflammatory action of this Ang degradation product, expanding the present view of the renin-angiotensin system.  (+info)

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 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.

Glutamyl Aminopeptidase (GAP, or sometimes also abbreviated as GP) is an enzyme that is found in many tissues throughout the body, including the kidneys and the intestines. Its primary function is to help break down proteins into smaller peptides and individual amino acids by removing certain types of amino acids from the ends of these protein chains.

GAP is a type of exopeptidase enzyme, which means that it works on the outside edges of proteins rather than in the middle. Specifically, GAP removes the amino acid glutamic acid (or its amide form, glutamine) from the N-terminus (the beginning end) of peptides and proteins.

In clinical settings, GAP is often measured in blood or urine samples as a biomarker for various medical conditions. For example, elevated levels of GAP in the blood may indicate liver disease or kidney damage, while decreased levels may be associated with certain types of cancer or gastrointestinal disorders. However, it's important to note that GAP is just one of many factors that doctors may consider when diagnosing and treating these conditions.

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.

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

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

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

Angiotensin 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.

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

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

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

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

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.

CD13, also known as aminopeptidase N, is a type of protein found on the surface of some cells in the human body. It is a type of antigen, which is a molecule that can trigger an immune response when recognized by the immune system. CD13 is found on the surface of various cell types, including certain white blood cells and cells that line the blood vessels. It plays a role in several biological processes, such as breaking down proteins and regulating inflammation.

CD13 is also a target for some cancer therapies because it is overexpressed in certain types of cancer cells. For example, CD13-targeted therapies have been developed to treat acute myeloid leukemia (AML), a type of blood cancer that affects the bone marrow. These therapies work by binding to CD13 on the surface of AML cells and triggering an immune response that helps to destroy the cancer cells.

It's important to note that while CD13 is an antigen, it is not typically associated with infectious diseases or foreign invaders, as other antigens might be. Instead, it is a normal component of human cells that can play a role in various physiological processes and disease states.

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

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

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

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

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

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

Natriuretic agents are substances that increase the secretion of sodium in the urine (natriuresis), which subsequently leads to a decrease in extracellular fluid volume and blood pressure. These agents can be endogenous, such as atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP), which are produced by the heart in response to increased stretching of cardiac muscle cells due to volume or pressure overload. Excessive production of these endogenous natriuretic peptides can contribute to the pathophysiology of heart failure.

Exogenous natriuretic agents, such as loop diuretics (e.g., furosemide), thiazide diuretics, and potassium-sparing diuretics, are used in clinical practice to treat conditions associated with fluid overload, like heart failure, liver cirrhosis, and kidney diseases. These medications act on different parts of the nephron to inhibit sodium reabsorption, thereby promoting natriuresis and diuresis.

Angiotensin amide is not a medical term itself, but it refers to a form of angiotensin II, which is a potent vasoconstrictor (a substance that narrows blood vessels) in the body. Angiotensin II is formed from angiotensin I through the action of an enzyme called angiotensin-converting enzyme (ACE).

Angiotensin II amide, also known as angiotensin II-amide or angiotensin II-(1-8), refers to the biologically active form of angiotensin II. It is an octapeptide with the amino acid sequence Asp-Arg-Val-Tyr-Ile-His-Pro-Phe, and its carboxy terminus is amidated (has an amide group instead of a free carboxyl group). This amide form of angiotensin II is more stable than the non-amidated form and has a longer half-life in circulation.

Angiotensin II amide plays a crucial role in regulating blood pressure and fluid balance by causing vasoconstriction, stimulating aldosterone release from the adrenal glands (which leads to sodium and water retention), and promoting thirst. Drugs that inhibit ACE or block angiotensin II receptors are commonly used in the treatment of hypertension and heart failure.

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

Gold compounds refer to chemical combinations in which gold atoms are bonded with other elements. In the context of medicine, particularly in the field of rheumatology, gold compounds have been used as disease-modifying antirheumatic drugs (DMARDs) for the treatment of conditions such as rheumatoid arthritis.

The most commonly used gold compound is auranofin, which contains gold in the +1 oxidation state. Auranofin is an oral medication that can help reduce inflammation and slow down joint damage caused by rheumatoid arthritis. It works by inhibiting certain enzymes involved in the inflammatory response.

Other gold compounds, such as sodium aurothiomalate and gold thioglucose, are administered parenterally (usually intramuscularly) and contain gold in the +3 oxidation state. These medications also have anti-inflammatory properties and can help alleviate symptoms of rheumatoid arthritis.

It is important to note that the use of gold compounds as a treatment for rheumatoid arthritis has declined over time due to their side effects, which may include kidney damage, skin reactions, mouth ulcers, and bone marrow suppression. They are generally reserved for patients who have not responded well to other DMARDs or biologic agents.

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

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

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

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."

I'm sorry for any confusion, but "sulfonic acids" are not a medical term. They are a type of compound in chemistry, specifically strong organic acids that contain the functional group -SO3H. Sulfonic acids are widely used in industry and research, including the production of detergents, dyes, and pharmaceuticals.

If you have any questions related to medical terminology or concepts, please don't hesitate to ask!

Aminopeptidases are a group of enzymes that catalyze the removal of amino acids from the N-terminus of polypeptides and proteins. They play important roles in various biological processes, including protein degradation, processing, and activation. Aminopeptidases are classified based on their specificity for different types of amino acids and the mechanism of their action. Some of the well-known aminopeptidases include leucine aminopeptidase, alanyl aminopeptidase, and arginine aminopeptidase. They are widely distributed in nature and found in various tissues and organisms, including bacteria, plants, and animals. In humans, aminopeptidases are involved in several physiological functions, such as digestion, immune response, and blood pressure regulation.

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

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.

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

Natriuresis is the process or condition of excreting an excessive amount of sodium (salt) through urine. It is a physiological response to high sodium levels in the body, which can be caused by various factors such as certain medical conditions (e.g., kidney disease, heart failure), medications, or dietary habits. The increased excretion of sodium helps regulate the body's water balance and maintain normal blood pressure. However, persistent natriuresis may indicate underlying health issues that require medical attention.

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.

I'm sorry for any confusion, but "Pyridines" is not a medical term. It is a chemical term that refers to a class of organic compounds with the chemical structure of a six-membered ring containing one nitrogen atom and five carbon atoms (heterocyclic aromatic compound).

In a biological or medical context, pyridine derivatives can be found in various natural and synthetic substances. For example, some medications contain pyridine rings as part of their chemical structure. However, "Pyridines" itself is not a medical term or condition.

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.

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.

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

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

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

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

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

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

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

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

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."

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

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

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

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

Methionine is an essential amino acid, which means that it cannot be synthesized by the human body and must be obtained through the diet. It plays a crucial role in various biological processes, including:

1. Protein synthesis: Methionine is one of the building blocks of proteins, helping to create new proteins and maintain the structure and function of cells.
2. Methylation: Methionine serves as a methyl group donor in various biochemical reactions, which are essential for DNA synthesis, gene regulation, and neurotransmitter production.
3. Antioxidant defense: Methionine can be converted to cysteine, which is involved in the formation of glutathione, a potent antioxidant that helps protect cells from oxidative damage.
4. Homocysteine metabolism: Methionine is involved in the conversion of homocysteine back to methionine through a process called remethylation, which is essential for maintaining normal homocysteine levels and preventing cardiovascular disease.
5. Fat metabolism: Methionine helps facilitate the breakdown and metabolism of fats in the body.

Foods rich in methionine include meat, fish, dairy products, eggs, and some nuts and seeds.

Renovascular hypertension is a type of secondary hypertension (high blood pressure) that is caused by renal artery stenosis or narrowing. This condition reduces blood flow to the kidneys, leading to the activation of the renin-angiotensin-aldosterone system (RAAS), which causes an increase in peripheral vascular resistance and blood volume, resulting in hypertension.

Renovascular hypertension is often seen in people with atherosclerosis or fibromuscular dysplasia, which are the most common causes of renal artery stenosis. Other conditions that can lead to renovascular hypertension include vasculitis, blood clots, and compression of the renal artery by nearby structures.

Diagnosis of renovascular hypertension typically involves imaging studies such as duplex ultrasound, CT angiography, or magnetic resonance angiography to visualize the renal arteries and assess for stenosis. Treatment may involve medications to control blood pressure, lifestyle modifications, and procedures such as angioplasty and stenting to open up the narrowed renal artery. In some cases, surgery may be necessary to restore blood flow to the kidney.

Renal artery obstruction is a medical condition that refers to the blockage or restriction of blood flow in the renal artery, which is the main vessel that supplies oxygenated and nutrient-rich blood to the kidneys. This obstruction can be caused by various factors, such as blood clots, atherosclerosis (the buildup of fats, cholesterol, and other substances in and on the artery walls), emboli (tiny particles or air bubbles that travel through the bloodstream and lodge in smaller vessels), or compressive masses like tumors.

The obstruction can lead to reduced kidney function, hypertension, and even kidney failure in severe cases. Symptoms may include high blood pressure, proteinuria (the presence of protein in the urine), hematuria (blood in the urine), and a decrease in kidney function as measured by serum creatinine levels. Diagnosis typically involves imaging studies like Doppler ultrasound, CT angiography, or magnetic resonance angiography to visualize the renal artery and assess the extent of the obstruction. Treatment options may include medications to control blood pressure and reduce kidney damage, as well as invasive procedures like angioplasty and stenting or surgical intervention to remove the obstruction and restore normal blood flow to the kidneys.

The renal artery is a pair of blood vessels that originate from the abdominal aorta and supply oxygenated blood to each kidney. These arteries branch into several smaller vessels that provide blood to the various parts of the kidneys, including the renal cortex and medulla. The renal arteries also carry nutrients and other essential components needed for the normal functioning of the kidneys. Any damage or blockage to the renal artery can lead to serious consequences, such as reduced kidney function or even kidney failure.

Arterial occlusive diseases are medical conditions characterized by the blockage or narrowing of the arteries, which can lead to a reduction in blood flow to various parts of the body. This reduction in blood flow can cause tissue damage and may result in serious complications such as tissue death (gangrene), organ dysfunction, or even death.

The most common cause of arterial occlusive diseases is atherosclerosis, which is the buildup of plaque made up of fat, cholesterol, calcium, and other substances in the inner lining of the artery walls. Over time, this plaque can harden and narrow the arteries, restricting blood flow. Other causes of arterial occlusive diseases include blood clots, emboli (tiny particles that travel through the bloodstream and lodge in smaller vessels), inflammation, trauma, and certain inherited conditions.

Symptoms of arterial occlusive diseases depend on the location and severity of the blockage. Common symptoms include:

* Pain, cramping, or fatigue in the affected limb, often triggered by exercise and relieved by rest (claudication)
* Numbness, tingling, or weakness in the affected limb
* Coldness or discoloration of the skin in the affected area
* Slow-healing sores or wounds on the toes, feet, or legs
* Erectile dysfunction in men

Treatment for arterial occlusive diseases may include lifestyle changes such as quitting smoking, exercising regularly, and eating a healthy diet. Medications to lower cholesterol, control blood pressure, prevent blood clots, or manage pain may also be prescribed. In severe cases, surgical procedures such as angioplasty, stenting, or bypass surgery may be necessary to restore blood flow.

Renal hypertension, also known as renovascular hypertension, is a type of secondary hypertension (high blood pressure) that is caused by narrowing or obstruction of the renal arteries or veins, which supply blood to the kidneys. This can lead to decreased blood flow and oxygen delivery to the kidney tissue, activating the renin-angiotensin-aldosterone system (RAAS) and resulting in increased peripheral vascular resistance, sodium retention, and extracellular fluid volume, ultimately causing hypertension.

Renal hypertension can be classified into two types:

1. Renin-dependent renal hypertension: This is caused by a decrease in blood flow to the kidneys, leading to increased renin release from the juxtaglomerular cells of the kidney. Renin converts angiotensinogen to angiotensin I, which is then converted to angiotensin II by angiotensin-converting enzyme (ACE). Angiotensin II is a potent vasoconstrictor that causes an increase in peripheral vascular resistance and blood pressure.
2. Renin-independent renal hypertension: This is caused by increased sodium retention and extracellular fluid volume, leading to an increase in blood pressure. This can be due to various factors such as obstructive sleep apnea, primary aldosteronism, or pheochromocytoma.

Renal hypertension is often asymptomatic but can lead to serious complications such as kidney damage, heart failure, and stroke if left untreated. Diagnosis of renal hypertension involves imaging studies such as renal artery duplex ultrasound, CT angiography, or magnetic resonance angiography (MRA) to identify any narrowing or obstruction in the renal arteries or veins. Treatment options include medications such as ACE inhibitors, angiotensin receptor blockers (ARBs), calcium channel blockers, and diuretics, as well as interventions such as angioplasty and stenting to improve blood flow to the kidneys.

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

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

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

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There are three isoforms of the peptide (identified as ET-1, -2, -3), each encoded by a separate gene, with varying regions of ... Agapitov AV, Haynes WG (March 2002). "Role of endothelin in cardiovascular disease". Journal of the Renin-Angiotensin- ... Endothelin receptors are present in the three pituitary lobes which display increased metabolic activity when exposed to ET-1 ... whereas the ETB receptor has the same affinity for all three ET peptides. The two types of ET receptor are distributed across ...
Pharmacophore There are three functional groups that are the most important parts for the bioactivity of ARBs, see figure 1 for ... 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- ...
... and three percent African ancestry. However, the study sampled only 19 people. A 2012 study published by the Journal of Human ... Journal of the Renin-Angiotensin-Aldosterone System. 12 (3): 231-237. doi:10.1177/1470320310388440. PMID 21163863. S2CID ... three to five percent) mtDNA. A Mexico City autosomal ancestry study found that the European ancestry of Mexicans was 52 ... "Genetic admixture in three mexican mestizo populations based on D1S80 and HLA-DQA1 Loci". American Journal of Human Biology. 14 ...
109 (23 Suppl 1): III-50-III-57. doi:10.1161/01.CIR.0000131519.15067.1f. PMID 15198967. Omar MA, Wilson JP (February 2002). " ... Drapala A, Sikora M, Ufnal M (September 2014). "Statins, the renin-angiotensin-aldosterone system and hypertension - a tale of ... A 2015 Cochrane systematic review update reported that rosuvastatin is more than three-fold more potent than atorvastatin. ... Adult Treatment Panel III): Executive Summary. Bethesda, MD: National Institutes of Health. National Heart, Lung, and Blood ...
People from the United States have moved too, now making up more than three-quarters of Mexico's roughly one million documented ... Journal of the Renin-Angiotensin-Aldosterone System. 12 (3): 231-237. doi:10.1177/1470320310388440. PMID 21163863. S2CID ... The field research consisted of three waves of interviews on different Mexican states during the timespan of a year, people ... It is concluded then, that across nearly three centuries of colonization, the population growth trends of whites and mestizos ...
I-II (illustrated, reprinted ed.). Cambridge University Press. p. 21. ISBN 978-0521245166. López-Calvo, Ignacio (2013). The ... Journal of the Renin-Angiotensin-Aldosterone System. 12 (3): 231-237. doi:10.1177/1470320310388440. PMID 21163863. S2CID ... Genetic studies in Mexico can be divided on three groups: studies made on self-identified Mestizos, studies made on Indigenous ... Sixty-two percent of the population over fifteen is married, three percent divorced and four percent widowed. However, younger ...
The aminopeptide sequence for saralasin differs from angiotensin II at three sites. At position 1, sarcosine replaces aspartic ... Ip S, Tsang S, Wong T, Che C, Leung P (2003). "Saralasin, a nonspecific angiotensin II receptor antagonist, attenuates ... Saralasin is a competitive angiotensin II receptor antagonist with partial agonist activity. ... the inhibitors of renin-angiotensin system, on cerulein-induced acute pancreatitis". Regul Pept. 111 (1-3): 47-53. doi:10.1016/ ...
Rössig L, Hermann C, Haendeler J, Assmus B, Zeiher AM, Dimmeler S (January 2002). "Angiotensin II-induced upregulation of MAP ... "Chromosomal localization of three human dual specificity phosphatase genes (DUSP4, DUSP6, and DUSP7)". Genomics. 42 (3): 524-7 ... Upregulation of MKP-3 has been shown to alleviate chronic postoperative pain. DUSP6 has been shown to interact with MAPK3. ... 82 (3-4): 156-9. doi:10.1159/000015091. PMID 9858808. S2CID 46883904. Stewart AE, Dowd S, Keyse SM, McDonald NQ (February 1999 ...
Overexpression of this gene in mammalian cells was reported to inhibit angiotensin-II induced cell calcium mobilization and ... in angiotensin-II signaling". Biochem. Biophys. Res. Commun. 283 (5): 1061-8. doi:10.1006/bbrc.2001.4881. PMID 11355880. Saha S ... 565 (1-3): 181-7. doi:10.1016/j.febslet.2004.03.062. PMID 15135076. S2CID 29552515. Wu X, Zeng H, Zhang X, et al. (2004). " ... 2004). "PRL-3 expression in metastatic cancers". Clin. Cancer Res. 9 (15): 5607-15. PMID 14654542. Kozlov G, Cheng J, Ziomek E ...
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 ...
Efficacy requires three key PD/PK areas at an effective level; the parameters of the three characteristics will need to be ... 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 ...
The enzyme degrades vasoconstricting angiotensin II into angiotensin III and therefore helps to regulate blood pressure. Reaux ... which generates one of the main effector peptides of the brain renin-angiotensin system, angiotensin III, has a key role in ...
The human AGTR2 gene is composed of three exons and spans at least 5 kb. Exons 1 and 2 encode for 5' untranslated mRNA sequence ... Angiotensin II receptor type 2 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. ...
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 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, ...
... by increase in the plasma concentration of angiotensin III. by increased plasma angiotensin II, ACTH, or potassium levels. The ... Control of aldosterone release from the adrenal cortex: The role of the renin-angiotensin system: Angiotensin is involved in ... Angiotensin II acts synergistically with potassium. The role of sympathetic nerves: Aldosterone production is also affected to ... Aldosterone synthase normally is not ACTH sensitive, and is only activated by angiotensin II.[citation needed] Aldosterone ...
Also able to cleave angiotensin III to generate angiotensin IV, a bioactive peptide of the renin-angiotensin pathway. Due to ... Chromosome 9 open reading frame 3 (C9ORF3) also known as aminopeptidase O (APO) is an enzyme which in humans is encoded by the ...
... (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 ...
It does so by inhibiting the enzymes aminopeptidase N (APN), dipeptidyl peptidase III (DPP3), angiotensin-converting enzyme ( ... 3) receptor antagonist". Journal of Medicinal Chemistry. 50 (18): 4543-7. doi:10.1021/jm070114m. PMID 17676725. (CS1 Japanese- ...
This protein may also be involved in blood pressure regulation by inactivation of angiotensin II. Three transcript variants ... 19 (3): 251-7. doi:10.1002/humu.10047. PMID 11857741. S2CID 23459237. Cui X, Hawari F, Alsaaty S, Lawrence M, Combs CA, Geng W ... 3 (12): 1169-76. doi:10.1038/ni859. PMID 12436109. S2CID 21648629. York IA, Chang SC, Saric T, Keys JA, Favreau JM, Goldberg AL ... 419 (6906): 480-3. doi:10.1038/nature01074. PMID 12368856. S2CID 4379291. Saric T, Chang SC, Hattori A, York IA, Markant S, ...
Angiotensin II -> Vasopressin) Increase PAI-1 and PAI-2 also through Angiotensin II Lipid Increase HDL, triglyceride Decrease ... There are three major endogenous estrogens that have estrogenic hormonal activity: estrone (E1), estradiol (E2), and estriol ( ... ISBN 978-0-32-367281-8. Estrogen is a generic term for any of three similar hormones derived from cholesterol: estradiol, ... Coagulation Increase circulating level of factors 2, 7, 9, 10, plasminogen Decrease antithrombin III Increase platelet ...
Angiotensin II-induced senescence of vascular smooth muscle cells requires down-regulation of ZnT-3 and ZnT-10. Solute carrier ... Patrushev N, Seidel-Rogol B, Salazar G (2012). "Angiotensin II requires zinc and downregulation of the zinc transporters ZnT3 ... In mice, ZnT-3 is required for some forms of memory that depend on the hippocampus and the amygdala. Zinc transport by ZnT-3 ... Zinc transporter 3 also known as solute carrier family 30 member 3 is a protein in humans that is encoded by the SLC30A3 gene. ...
4-trisphosphate to a new tetrakisphosphate isomer in angiotensin-stimulated adrenal glomerulosa cells". J. Biol. Chem. 262 (21 ... J. 351 (Pt 3): 551-5. doi:10.1042/0264-6021:3510551. PMC 1221393. PMID 11042108. Vogel G, Riley AM, Potter BV, Shears SB (2002 ... Yang X, Shears SB (2000). "Multitasking in signal transduction by a promiscuous human Ins(3,4,5,6)P(4) 1-kinase/Ins(1,3,4)P(3) ... As of late 2007, 3 structures have been solved for this class of enzymes, with PDB accession codes 2ODT, 2Q7D, and 2QB5. ...
Alvarez BV, Fujinaga J, Casey JR (2002). "Molecular basis for angiotensin II-induced increase of chloride/bicarbonate exchange ... Anion exchange protein 3 is a membrane transport protein that in humans is encoded by the SLC4A3 gene. AE3 is functionally ... 297 (3): C526-36. doi:10.1152/ajpcell.00572.2008. PMID 19605733. S2CID 29802528. Alper SL, Darman RB, Chernova MN, Dahl NK ( ... 22 (3): 605-9. doi:10.1006/geno.1994.1433. PMID 8001971. "Entrez Gene: SLC4A3 solute carrier family 4, anion exchanger, member ...
This leads to the product angiotensin I (Ang I) which is a decapeptide. Ang I is broken down by the angiotensin-converting ... There are four S pockets, and three S′ pockets (table 1). The pockets alternate on either side of the backbone in the ligand. ... Ferrario, C. M.; Iyer, S. N. (1998). "angiotensin-(1-7): A bioactive fragment of the renin-angiotensin system". Regulatory ... design Angiotensin Angiotensin II receptor antagonist Beta blocker Circulatory system Discovery and development of angiotensin ...
... increased activity of the Renin-angiotensin-aldosterone system. Extracellular fluid Veins "Edema and Related Medical Conditions ...
There are three volume regulating systems: two salt saving systems, the renin angiotensin aldosterone system (RAAS) and the ... ANP has the opposite effect of angiotensin II on the kidney: angiotensin II increases renal sodium retention and ANP increases ... ANP inhibits the effect of Angiotensin II on the mesangial cells, thereby relaxing them. ANP increases the radius and number of ... Other dual inhibitors of NEP with ACE/angiotensin receptor are (in 2003) being developed by pharmaceutical companies. ANP is ...
"SMAD3 deficiency promotes inflammatory aortic aneurysms in angiotensin II-infused mice via activation of iNOS". Journal of the ... The MH1 structure consists of four-helices and three sets of antiparallel β-hairpins, one of which is used to interact with DNA ... the three residues strictly conserved in all R-SMADS and in SMAD4 (Arg74 and Gln76 located in β2 and Lys81 in β3 in SMAD3) ... underlining the critical roles of these three proteins within the TGF-β signaling pathway and the impact of this pathway in ...
... which cleaves C-terminal amino acids linked to proline in peptides such as angiotensin II, III and des-Arg9-bradykinin. The ... The importance of angiotensin II, one of the substrates of this enzyme, in regulating blood pressure and electrolyte balance ... Yang HY, Erdös EG, Chiang TS (1968). "New enzymatic route for the inactivation of angiotensin". Nature. 218 (5148): 1224-6. ... 44 (3): 365-7. doi:10.1006/geno.1997.4883. PMID 9325062. Shariat-Madar Z, Mahdi F, Schmaier AH (2002). "Identification and ...
Angiotensin III increases blood pressure and stimulates aldosterone secretion from the adrenal cortex; it has 100% ... 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 ...
keywords = "Angiotensin, Dermal, Diabetes, NorLeu3-angiotensin 1-7, Wound healing",. author = "Kathleen Rodgers and Shelagh ... This review provides an overview of the development of NorLeu3-angiotensin (1-7) (NorLeu3-A(1-7)) as an active agent for the ... This review provides an overview of the development of NorLeu3-angiotensin (1-7) (NorLeu3-A(1-7)) as an active agent for the ... This review provides an overview of the development of NorLeu3-angiotensin (1-7) (NorLeu3-A(1-7)) as an active agent for the ...
Angiotensin, the principal stress component of the renin-angiotensin aldosterone system (RAAS), plays an important role in the ... angiotensin, and aldosterone. Angiotensin raises blood pressure by a number of actions, with the most important ones being ... The concentrations of angiotensin, C-reactive protein (CRP), interleukin-8 (IL-8), and tumor necrosis factor-alpha (TNF-α) were ... The concentrations of angiotensin, C-reactive protein (CRP), interleukin-8 (IL-8), and tumor necrosis factor-alpha (TNF-α) were ...
Prevents conversion of angiotensin I to angiotensin II, which is a potent vasoconstrictor. Also causes lower aldosterone ... Nonpeptide angiotensin II receptor antagonist that blocks the vasoconstrictor and aldosterone-secreting effects of angiotensin ... Angiotensin-converting enzyme inhibitors. Class Summary. Comparative studies show ACE inhibitors are more effective than other ... Angiotensin II receptor antagonists. Class Summary. Reduce blood pressure and proteinuria, protect renal function, and delay ...
The study was performed to investigate the association of interleukin 17 (IL 17) or angiotensin II (Ang II) with refractory ... Association of interleukin 17 / angiotensin II with refractory hypertension risk in hemodialysis patients. ... Association of interleukin 17 / angiotensin II with refractory hypertension risk in hemodi ...
Renin/Angiotensin (RAS) Cascade (3) Tags (1) Tissue Remodeling/MMPs (12) Virology (4) ...
Of the three patterns, DD is associated with the highest levels of angiotensin-converting enzyme. The DD pattern is thought to ... which converts a hormone called angiotensin I to another form called angiotensin II. Angiotensin II helps control blood ... The ACE gene provides instructions for making a protein called angiotensin-converting enzyme, ... A variant in this gene, called R577X, leads to production of an abnormally short α-actinin-3 protein that is quickly broken ...
We tested the hypothesis that angiotensin II-induced increases in oxidative stress impair cutaneous perfusion and swea … ... It is unclear if angiotensin II, which can increase the production of reactive oxygen species (oxidative stress), modulates ... When ascorbate was coinfused with angiotensin II, the effect of angiotensin II on sweating was abolished (all P , 0.05); ... Compared with control, angiotensin II reduced both CVC and sweating at baseline resting and during each recovery in the heat ( ...
During 2008-2011, 87 stx2f STEC infections were registered in the Netherlands (3). These infections were relatively mild; no ... To improve proteinuria, physicians prescribed a 3-month course of angiotensin-converting enzyme inhibitors after discharge. ... 3). Besides being detected in humans, stx2f STEC has only been detected in pigeons (6). ...
Angiotensin-Converting Enzyme 3 (ACE3) Protects Against Pressure Overload-Induced Cardiac Hypertrophy. J Am Heart Assoc. 2016 5 ... Type III Transforming Growth Factor-beta Receptor Drives Cardiac Hypertrophy Through beta-Arrestin2-Dependent Activation of ... Nerve stimulation induced overflow of neuropeptide Y and modulation by angiotensin II in spontaneously hypertensive rats. Am J ... NPY or angiotensin II (Ang II) was used to trigger CH model in vitro in neonatal rat ventricular myocytes (NRVMs). We found ...
Adherence to Renin-Angiotensin System Antagonist (n = 967). Adherence to Statins (n = 1,034). Use of High-Risk Medicationsb (n ... Adherence to Renin-Angiotensin System Antagonist Medications. Adherence to Statins. Use of High-Risk Medicationsb (≥65 y). ... Renin-Angiotensin System Antagonist Adherence. Statin Adherence. Use of High-Risk Medicationsb. Statin Use in Persons with ... We evaluated adherence for noninsulin diabetes medications, renin-angiotensin system antagonists, and statins, as well as ...
... such as angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs), did not have higher ... Life sciences/Biochemistry/Biomolecules/Enzymes/Angiotensin converting enzyme 2 * /Health and medicine/Diseases and disorders/ ... image: The role of ACE2 in controlling the renin-angiotensin system and the proteolytic shedding of membrane-bound ACE2 by ADAM ... Evidence from a large study of several thousand patients shows that men have higher concentrations of angiotensin-converting ...
2019-novel coronavirus infection in a three-month-old baby. Zhonghua Za Zhi. (2020) 58:E006. doi: 10.3760/cma.j.issn.0578- ... Higher levels of angiotensin II are also proposed to be related to acute lung injury (3). Meanwhile, non-survivors are ... Clinical features and multidisciplinary treatment outcome of COVID-19 pneumonia: a report of three cases. J Formosan Med Assoc ... Dynamic chest ct evaluation in three cases of 2019 novel coronavirus pneumonia. Arch Iranian Med. (2020) 23:277-80. doi: ...
III. Histopathological and electrocardiographical responses to chronic infection. Am J Trop Med Hyg. 1987;37(3):541-549. ... J Renin Angiotensin Aldosterone Syst. 2006;7(3):162-167.. 68.. Bilate AM, Teixeira PC, Ribeiro SP, et al. Distinct outcomes of ... 94 GI alterations were observed in capuchin monkeys infected with three T. cruzi strains (CA1, Colombian, or Tulahuen). ... Table 3 Some factors related to variability in experimental conditions in in vivo models. Abbreviation: PCR, polymerase chain ...
Dopaminergic Control of Aldosterone Secretion is Independent of the Renin-Angiotensin System in Rats J. R. Sowers; J. R. Sowers ... Pre-administration of angiotensin converting enzyme inhibitor, captopril (SQ 14 225) and the angiotensin II antagonist, ... Dopaminergic Control of Aldosterone Secretion is Independent of the Renin-Angiotensin System in Rats. Clin Sci (Lond) 1 ... Thus dopaminergic modulation of aldosterone secretion occurs independently of alterations in the renin-angiotensin system. ...
RVHT is the clinical consequence of renin-angiotensin-aldosterone activation as a result of renal ischemia. ... such as captopril prevents the conversion of angiotensin I to the active vasoconstrictors angiotensin II and angiotensin III. ... Three-dimensional phase-contrast magnetic resonance angiographic (MRA) images of normal renal arteries. View Media Gallery ... The effect of the angiotensin-converting enzyme (ACE) inhibitor captopril on RAS was first described by Majd et al. [44] They ...
However, ACE2 is not only a SARS-CoV-2 receptor but also regulates the renin-angiotensin system (RAS), which has significant ... 4. Aleksova A, Gagno G, Sinagra G, Effects of SARS-CoV-2 on cardiovascular system: The dual role of angiotensin-converting ... protein to the angiotensin-converting enzyme 2 (ACE2) receptor [3]. The binding of the S protein to the ACE2 receptor is ... 3. Jackson CB, Farzan M, Chen B, Choe H, Mechanisms of SARS-CoV-2 entry into cells: Nat Rev Mol Cell Biol, 2022; 23(1); 3-20 ...
The expression of the intrarenal renin angiotensin mRNAs in Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) ... Three protocols were used 1) control (n = 6), 2) converting-enzyme inhibition (CEI, n = 6), and 3) CEI combined with a constant ... In one set of experiments we measured the SFP feedback response to changes in loop perfusion at three levels of arterial ... In other experiments arterial pressure was altered while loop perfusion rate was fixed at one of three levels. Without loop ...
Cravedi P, Ruggenenti P, Remuzzi G. Intensified inhibition of renin-angiotensin system: A way to improve renal protection? ... Maximizing renin-angiotensin system (RAS) blockade through combined ACE inhibitor and ARB therapy has been shown to further ... Maximizing renin-angiotensin system (RAS) blockade through combined ACE inhibitor and ARB therapy has been shown to further ... Maximizing renin-angiotensin system (RAS) blockade through combined ACE inhibitor and ARB therapy has been shown to further ...
In the broad range of known bioactive peptides, angiotensin I-converting enzyme inhibitory (ACEI) peptides derived from food ... Another example that gathered mediatic exposure was ZMapp, a cocktail of three chimeric monoclonal antibodies targeting the ... showed high levels of inhibition of the angiotensin-converting enzyme, with an IC50 value of 3.5 μg ml−1, and 10-fold lower ... Lee S-H, Qian Z-J, Kim S-K. A novel angiotensin I converting enzyme inhibitory peptide from tuna frame protein hydrolysate and ...
Identified substrates of aminopeptidase N include the angiotensin I-III peptide hormones, the opioid peptide met-enkephalin, ...
... one and three deaths in the C21 and placebo group, respectively). Treatment with C21 was safe and well tolerated. ... de Man FS, Tu L, Handoko ML, Rain S, Ruiter G, Francois C, et al. Dysregulated renin-angiotensin-aldosterone system contributes ... Rathinasabapathy A, Horowitz A, Horton K, Kumar A, Gladson S, Unger T, et al. The Selective Angiotensin II Type 2 Receptor ... Bruce E, Shenoy V, Rathinasabapathy A, Espejo A, Horowitz A, Oswalt A, et al. Selective activation of angiotensin AT2 receptors ...
Angiotensin III. Angiotensin III has mild vasopressor capabilities, but almost 100% of the aldosterone producing effects on the ... Angiotensin II. Angiotensin I is converted by an angiotensin converting enzyme (ACE) into angiotensin II. ACE is found in ... Angiotensin I. Angiotensin I has limited known effects on the human body, other than being a precursor to angiotensin II. ... When Angiotensinogen combines with renin the enzyme angiotensin is produced.. Angiotensin. Angiotensin is an oligopeptide found ...
We considered the data of a subset of Brisighella Heart Study (BHS) participants who were consecutively evaluated in three ... angiotensin II receptor blockers (ARBs), calcium-channel blockers (CCB) and/or thiazide/thiazide-like diuretics. The remaining ... The combination treatment with renin-angiotensin system (RAS) modulators, CCBs and thiazide/thiazide-like diuretics was ... Cited by 3 , Viewed by 1437 Abstract Sacubitril/valsartan represents the combination that became "sine qua non" in the ...
XFEL structure of human angiotensin II type 2 receptor (Orthorhombic form) in complex with compound 1 (N-benzyl-N-(2-ethyl-4- ... oxo-3-{[2-(2H-tetrazol-5-yl)[1,1-biphenyl]-4-yl] methyl}-3,4-dihydroquinazolin-6-yl)thiophene-2-carboxamide) ... The angiotensin II receptors AT 1 R and AT 2 R serve as key components of the renin-angiotensin-aldosterone system. AT 1 R has ... Structural basis for selectivity and diversity in angiotensin II receptors.. Zhang, H., Han, G.W., Batyuk, A., Ishchenko, A., ...
Evaluation of the renin-angiotensin system in cardiac tissues of cats with pressure-overload cardiac hypertrophy ... https://avmajournals.avma.org/abstract/journals/ajvr/63/3/ajvr.2002.63.312.xml. The link was not copied. Your current browser ...
McQueen, J. & Semple, P. (1991). Angiotensin Receptor Assay and Characterization. Methods in Neurosciences, Academic Press, 5( ... DNA spots had to pass three quality control tests *Signal intensity had to be significantly greater than the intensity of the ... Three micrograms of mRNA were labeled by incorporating Cy3- and Cy5-dCTP through reverse transcription ... At 10 minutes, 30 minutes, or 60 hours there were three replicates ...
Angiotensin 2 Receptor Blockers Category Drug Index Pediatric Oncall ...
It seems to lower angiotensin ii levels, get rid of stress hormones cortisol and norepinephrine, and generally boosts mood. ... These three things I listed in my own theoretical order of importance. ... Vitamin D is a great renin angiotensin aldosterone regulator and can have many other beneficial effects as well. ...

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