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.
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 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.
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.
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 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.
Persistently high systemic arterial BLOOD PRESSURE. Based on multiple readings (BLOOD PRESSURE DETERMINATION), hypertension is currently defined as when SYSTOLIC PRESSURE is consistently greater than 140 mm Hg or when DIASTOLIC PRESSURE is consistently 90 mm Hg or more.
A 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 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.
PRESSURE of the BLOOD on the ARTERIES and other BLOOD VESSELS.
The 3-methyl ether of ETHINYL ESTRADIOL. It must be demethylated to be biologically active. It is used as the estrogen component of many combination ORAL CONTRACEPTIVES.
RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.
Cell surface proteins that bind ANGIOTENSINS and trigger intracellular changes influencing the behavior of cells.
Body organ that filters blood for the secretion of URINE and that regulates ion concentrations.
The regular and simultaneous occurrence in a single interbreeding population of two or more discontinuous genotypes. The concept includes differences in genotypes ranging in size from a single nucleotide site (POLYMORPHISM, SINGLE NUCLEOTIDE) to large nucleotide sequences visible at a chromosomal level.
A synthetic hormone used for androgen replacement therapy and as an hormonal antineoplastic agent (ANTINEOPLASTIC AGENTS, HORMONAL).
An angiotensin receptor subtype that is expressed at high levels in fetal tissues. Many effects of the angiotensin type 2 receptor such as VASODILATION and sodium loss are the opposite of that of the ANGIOTENSIN TYPE 1 RECEPTOR.
ANIMALS whose GENOME has been altered by GENETIC ENGINEERING, or their offspring.
The genetic constitution of the individual, comprising the ALLELES present at each GENETIC LOCUS.
An antagonist of ANGIOTENSIN TYPE 1 RECEPTOR with antihypertensive activity due to the reduced pressor effect of ANGIOTENSIN II.
A strain of Rattus norvegicus used as a normotensive control for the spontaneous hypertensive rats (SHR).
A strain of Rattus norvegicus with elevated blood pressure used as a model for studying hypertension and stroke.
Laboratory rats that have been produced from a genetically manipulated rat EGG or rat EMBRYO, MAMMALIAN. They contain genes from another species.
The renal tubule portion that extends from the BOWMAN CAPSULE in the KIDNEY CORTEX into the KIDNEY MEDULLA. The proximal tubule consists of a convoluted proximal segment in the cortex, and a distal straight segment descending into the medulla where it forms the U-shaped LOOP OF HENLE.
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.
One of several basic proteins released from EOSINOPHIL cytoplasmic granules. Eosinophil major basic protein is a 14-kDa cytotoxic peptide with a pI of 10.9. In addition to its direct cytotoxic effects, it stimulates the release of variety of INFLAMMATION MEDIATORS.
A structure, situated close to the intraventricular foramen, which induces DRINKING BEHAVIOR after stimulation with ANGIOTENSIN II.
Variant forms of the same gene, occupying the same locus on homologous CHROMOSOMES, and governing the variants in production of the same gene product.
Agents that antagonize ANGIOTENSIN II TYPE 1 RECEPTOR. Included are ANGIOTENSIN II analogs such as SARALASIN and biphenylimidazoles such as LOSARTAN. Some are used as ANTIHYPERTENSIVE AGENTS.
Sodium chloride used in foods.
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.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control (induction or repression) of gene action at the level of transcription or translation.
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.
Excision of kidney.
A chronic form of glomerulonephritis characterized by deposits of predominantly IMMUNOGLOBULIN A in the mesangial area (GLOMERULAR MESANGIUM). Deposits of COMPLEMENT C3 and IMMUNOGLOBULIN G are also often found. Clinical features may progress from asymptomatic HEMATURIA to END-STAGE KIDNEY DISEASE.
The proportion of one particular in the total of all ALLELES for one genetic locus in a breeding POPULATION.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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.

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.

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.

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."

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.

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.

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.

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 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.

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.

Mestranol is a synthetic form of estrogen, which is a female sex hormone used in oral contraceptives and hormone replacement therapy. It works by preventing the release of an egg from the ovary (ovulation) and altering the cervical mucus and the lining of the uterus to make it more difficult for sperm to reach the egg or for an already established pregnancy to be implanted.

Mestranol is typically combined with a progestin in birth control pills, such as those known as the "combined oral contraceptives." It's important to note that mestranol has largely been replaced by ethinyl estradiol, which is a more commonly used form of synthetic estrogen in hormonal medications.

As with any medication, there are potential risks and side effects associated with the use of mestranol, including an increased risk of blood clots, stroke, and certain types of cancer. It's essential to consult with a healthcare provider before starting or changing any hormonal medication.

Messenger RNA (mRNA) is a type of RNA (ribonucleic acid) that carries genetic information copied from DNA in the form of a series of three-base code "words," each of which specifies a particular amino acid. This information is used by the cell's machinery to construct proteins, a process known as translation. After being transcribed from DNA, mRNA travels out of the nucleus to the ribosomes in the cytoplasm where protein synthesis occurs. Once the protein has been synthesized, the mRNA may be degraded and recycled. Post-transcriptional modifications can also occur to mRNA, such as alternative splicing and addition of a 5' cap and a poly(A) tail, which can affect its stability, localization, and translation efficiency.

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.

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.

Genetic polymorphism refers to the occurrence of multiple forms (called alleles) of a particular gene within a population. These variations in the DNA sequence do not generally affect the function or survival of the organism, but they can contribute to differences in traits among individuals. Genetic polymorphisms can be caused by single nucleotide changes (SNPs), insertions or deletions of DNA segments, or other types of genetic rearrangements. They are important for understanding genetic diversity and evolution, as well as for identifying genetic factors that may contribute to disease susceptibility in humans.

Methyltestosterone is a synthetic form of the hormone testosterone, which is primarily used in the treatment of low testosterone levels (hypogonadism) in men. It has a methyl group attached to it, which allows it to be taken orally and still have significant effects on the body.

Testosterone is an androgen hormone that plays important roles in the development and maintenance of male sex characteristics, such as deepening of the voice, growth of facial and body hair, and increased muscle mass. It also helps maintain bone density, red blood cell production, and sex drive.

Methyltestosterone is available in various forms, including tablets and capsules, and its use should be under the supervision of a healthcare professional due to potential side effects and risks associated with its use, such as liver toxicity, increased risk of cardiovascular events, and changes in cholesterol levels.

It's important to note that methyltestosterone is not approved for use in women, as it can cause virilization (development of male sex characteristics) and other side effects.

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.

Genetically modified animals (GMAs) are those whose genetic makeup has been altered using biotechnological techniques. This is typically done by introducing one or more genes from another species into the animal's genome, resulting in a new trait or characteristic that does not naturally occur in that species. The introduced gene is often referred to as a transgene.

The process of creating GMAs involves several steps:

1. Isolation: The desired gene is isolated from the DNA of another organism.
2. Transfer: The isolated gene is transferred into the target animal's cells, usually using a vector such as a virus or bacterium.
3. Integration: The transgene integrates into the animal's chromosome, becoming a permanent part of its genetic makeup.
4. Selection: The modified cells are allowed to multiply, and those that contain the transgene are selected for further growth and development.
5. Breeding: The genetically modified individuals are bred to produce offspring that carry the desired trait.

GMAs have various applications in research, agriculture, and medicine. In research, they can serve as models for studying human diseases or testing new therapies. In agriculture, GMAs can be developed to exhibit enhanced growth rates, improved disease resistance, or increased nutritional value. In medicine, GMAs may be used to produce pharmaceuticals or other therapeutic agents within their bodies.

Examples of genetically modified animals include mice with added genes for specific proteins that make them useful models for studying human diseases, goats that produce a human protein in their milk to treat hemophilia, and pigs with enhanced resistance to certain viruses that could potentially be used as organ donors for humans.

It is important to note that the use of genetically modified animals raises ethical concerns related to animal welfare, environmental impact, and potential risks to human health. These issues must be carefully considered and addressed when developing and implementing GMA technologies.

Genotype, in genetics, refers to the complete heritable genetic makeup of an individual organism, including all of its genes. It is the set of instructions contained in an organism's DNA for the development and function of that organism. The genotype is the basis for an individual's inherited traits, and it can be contrasted with an individual's phenotype, which refers to the observable physical or biochemical characteristics of an organism that result from the expression of its genes in combination with environmental influences.

It is important to note that an individual's genotype is not necessarily identical to their genetic sequence. Some genes have multiple forms called alleles, and an individual may inherit different alleles for a given gene from each parent. The combination of alleles that an individual inherits for a particular gene is known as their genotype for that gene.

Understanding an individual's genotype can provide important information about their susceptibility to certain diseases, their response to drugs and other treatments, and their risk of passing on inherited genetic disorders to their offspring.

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."

WKY (Wistar Kyoto) is not a term that refers to "rats, inbred" in a medical definition. Instead, it is a strain of laboratory rat that is widely used in biomedical research. WKY rats are an inbred strain, which means they are the result of many generations of brother-sister matings, resulting in a genetically uniform population.

WKY rats originated from the Wistar Institute in Philadelphia and were established as a normotensive control strain to contrast with other rat strains that exhibit hypertension. They have since been used in various research areas, including cardiovascular, neurological, and behavioral studies. Compared to other commonly used rat strains like the spontaneously hypertensive rat (SHR), WKY rats are known for their lower blood pressure, reduced stress response, and greater emotionality.

In summary, "WKY" is a designation for an inbred strain of laboratory rat that is often used as a control group in biomedical research due to its normotensive characteristics.

SHR (Spontaneously Hypertensive Rats) are an inbred strain of rats that were originally developed through selective breeding for high blood pressure. They are widely used as a model to study hypertension and related cardiovascular diseases, as well as neurological disorders such as stroke and dementia.

Inbred strains of animals are created by mating genetically identical individuals (siblings or offspring) for many generations, resulting in a population that is highly homozygous at all genetic loci. This means that the animals within an inbred strain are essentially genetically identical to one another, which makes them useful for studying the effects of specific genes or environmental factors on disease processes.

SHR rats develop high blood pressure spontaneously, without any experimental manipulation, and show many features of human hypertension, such as increased vascular resistance, left ventricular hypertrophy, and renal dysfunction. They also exhibit a number of behavioral abnormalities, including hyperactivity, impulsivity, and cognitive deficits, which make them useful for studying the neurological consequences of hypertension and other cardiovascular diseases.

Overall, inbred SHR rats are an important tool in biomedical research, providing a valuable model for understanding the genetic and environmental factors that contribute to hypertension and related disorders.

Transgenic rats are genetically modified rats that have incorporated foreign DNA (transgene) into their own genome. This is typically done through the use of recombinant DNA techniques in the laboratory. The transgene can come from any species, including other mammals, plants, or even bacteria. Once the transgene is introduced into the rat's embryonic cells, it becomes a permanent part of the rat's genetic makeup and is passed on to its offspring.

Transgenic rats are used in biomedical research as models for studying human diseases, developing new therapies, and testing the safety and efficacy of drugs. They offer several advantages over traditional laboratory rats, including the ability to manipulate specific genes, study gene function and regulation, and investigate the underlying mechanisms of disease.

Some common applications of transgenic rats in research include:

1. Modeling human diseases: Transgenic rats can be engineered to develop symptoms and characteristics of human diseases, such as cancer, diabetes, Alzheimer's, and Parkinson's. This allows researchers to study the disease progression, test new treatments, and evaluate their effectiveness.
2. Gene function and regulation: By introducing specific genes into rats, scientists can investigate their role in various biological processes, such as development, aging, and metabolism. They can also study how genes are regulated and how they interact with each other.
3. Drug development and testing: Transgenic rats can be used to test the safety and efficacy of new drugs before they are tested in humans. By studying the effects of drugs on transgenic rats, researchers can gain insights into their potential benefits and risks.
4. Toxicology studies: Transgenic rats can be used to study the toxicity of chemicals, pollutants, and other substances. This helps ensure that new products and treatments are safe for human use.

In summary, transgenic rats are genetically modified rats that have incorporated foreign DNA into their own genome. They are widely used in biomedical research to model human diseases, study gene function and regulation, develop new therapies, and test the safety and efficacy of drugs.

The proximal kidney tubule is the initial portion of the renal tubule in the nephron of the kidney. It is located in the renal cortex and is called "proximal" because it is closer to the glomerulus, compared to the distal tubule. The proximal tubule plays a crucial role in the reabsorption of water, electrolytes, and nutrients from the filtrate that has been formed by the glomerulus. It also helps in the secretion of waste products and other substances into the urine.

The proximal tubule is divided into two segments: the pars convoluta and the pars recta. The pars convoluta is the curved portion that receives filtrate from the Bowman's capsule, while the pars recta is the straight portion that extends deeper into the renal cortex.

The proximal tubule is lined with a simple cuboidal epithelium, and its cells are characterized by numerous mitochondria, which provide energy for active transport processes. The apical surface of the proximal tubular cells has numerous microvilli, forming a brush border that increases the surface area for reabsorption.

In summary, the proximal kidney tubule is a critical site for the reabsorption of water, electrolytes, and nutrients from the glomerular filtrate, contributing to the maintenance of fluid and electrolyte balance in the body.

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.

Eosinophil Major Basic Protein (eMBP) is a cytotoxic protein found in the granules of eosinophils, which are a type of white blood cell that plays a role in the immune response, particularly against parasitic infections. eMBP is one of the four major basic proteins (MBPs) and is released during degranulation of eosinophils, a process that occurs in response to certain stimuli such as allergens or parasites.

eMBP has been found to have several biological activities, including direct toxicity to various cells, including parasites, mast cells, and airway epithelial cells. It can also induce the production of pro-inflammatory cytokines and chemokines, contributing to the inflammation observed in diseases such as asthma and allergies.

It is important to note that while eMBP has been extensively studied for its role in immunity and disease, further research is needed to fully understand its mechanisms of action and potential therapeutic applications.

The subfornical organ is a circumventricular organ located in the rostral part of the anterior wall of the third ventricle, above the fornix and posterior to the anterior commissure. It is one of the key structures involved in the regulation of fluid balance and cardiovascular function.

The subfornical organ contains specialized neurons that are sensitive to angiotensin II, a hormone that regulates blood pressure and fluid balance by stimulating thirst and vasopressin release. These neurons are not protected by the blood-brain barrier, allowing them to directly detect changes in circulating levels of angiotensin II and other substances.

The subfornical organ also contains receptors for other hormones and neurotransmitters that regulate fluid balance and cardiovascular function, such as atrial natriuretic peptide (ANP) and nitric oxide. These receptors allow the subfornical organ to integrate information from multiple sources and modulate its responses accordingly.

Overall, the subfornical organ plays a critical role in maintaining fluid balance and cardiovascular homeostasis by detecting changes in circulating hormones and neurotransmitters and initiating appropriate physiological responses.

An allele is a variant form of a gene that is located at a specific position on a specific chromosome. Alleles are alternative forms of the same gene that arise by mutation and are found at the same locus or position on homologous chromosomes.

Each person typically inherits two copies of each gene, one from each parent. If the two alleles are identical, a person is said to be homozygous for that trait. If the alleles are different, the person is heterozygous.

For example, the ABO blood group system has three alleles, A, B, and O, which determine a person's blood type. If a person inherits two A alleles, they will have type A blood; if they inherit one A and one B allele, they will have type AB blood; if they inherit two B alleles, they will have type B blood; and if they inherit two O alleles, they will have type O blood.

Alleles can also influence traits such as eye color, hair color, height, and other physical characteristics. Some alleles are dominant, meaning that only one copy of the allele is needed to express the trait, while others are recessive, meaning that two copies of the allele are needed to express the trait.

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.

Sodium chloride, commonly known as salt, is an essential electrolyte in dietary intake. It is a chemical compound made up of sodium (Na+) and chloride (Cl-) ions. In a medical context, particularly in nutrition and dietetics, "sodium chloride, dietary" refers to the consumption of this compound in food sources.

Sodium plays a crucial role in various bodily functions such as maintaining fluid balance, assisting nerve impulse transmission, and contributing to muscle contraction. The Dietary Guidelines for Americans recommend limiting sodium intake to less than 2,300 milligrams (mg) per day and further suggest an ideal limit of no more than 1,500 mg per day for most adults, especially those with high blood pressure. However, the average American consumes more than twice the recommended amount, primarily from processed and prepared foods. Excessive sodium intake can lead to high blood pressure and increase the risk of heart disease and stroke.

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.

'Gene expression regulation' refers to the processes that control whether, when, and where a particular gene is expressed, meaning the production of a specific protein or functional RNA encoded by that gene. This complex mechanism can be influenced by various factors such as transcription factors, chromatin remodeling, DNA methylation, non-coding RNAs, and post-transcriptional modifications, among others. Proper regulation of gene expression is crucial for normal cellular function, development, and maintaining homeostasis in living organisms. Dysregulation of gene expression can lead to various diseases, including cancer and genetic disorders.

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.

Nephrectomy is a surgical procedure in which all or part of a kidney is removed. It may be performed due to various reasons such as severe kidney damage, kidney cancer, or living donor transplantation. The type of nephrectomy depends on the reason for the surgery - a simple nephrectomy involves removing only the affected portion of the kidney, while a radical nephrectomy includes removal of the whole kidney along with its surrounding tissues like the adrenal gland and lymph nodes.

IGA glomerulonephritis (also known as Berger's disease) is a type of glomerulonephritis, which is a condition characterized by inflammation of the glomeruli, the tiny filtering units in the kidneys. In IgA glomerulonephritis, the immune system produces an abnormal amount of IgA antibodies, which deposit in the glomeruli and cause inflammation. This can lead to symptoms such as blood in the urine, protein in the urine, and swelling in the legs and feet. In some cases, it can also lead to kidney failure. The exact cause of IgA glomerulonephritis is not known, but it is often associated with other conditions such as infections, autoimmune diseases, and certain medications.

Gene frequency, also known as allele frequency, is a measure in population genetics that reflects the proportion of a particular gene or allele (variant of a gene) in a given population. It is calculated as the number of copies of a specific allele divided by the total number of all alleles at that genetic locus in the population.

For example, if we consider a gene with two possible alleles, A and a, the gene frequency of allele A (denoted as p) can be calculated as follows:

p = (number of copies of allele A) / (total number of all alleles at that locus)

Similarly, the gene frequency of allele a (denoted as q) would be:

q = (number of copies of allele a) / (total number of all alleles at that locus)

Since there are only two possible alleles for this gene in this example, p + q = 1. These frequencies can help researchers understand genetic diversity and evolutionary processes within populations.

"Interleukin-6 Mediates Angiotensinogen Gene Expression during Liver Regeneration". PLOS ONE. 8 (7): e67868. Bibcode:2013PLoSO ... Dzau, VJ; Herrmann, HC (15-22 February 1982). "Hormonal control of angiotensinogen production". Life Sciences. 30 (7-8): 577-84 ... Angiotensinogen expression Regenerate itself by hepatocyte mitosis Via STAT and Gab1: RAS/MAPK, PLC/IP3 and PI3K/FAK Cell ...
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Dickson ME, Sigmund CD (July 2006). "Genetic basis of hypertension: revisiting angiotensinogen". Hypertension. 48 (1): 14-20. ...
One of these genes is the angiotensinogen (AGT) gene, studied extensively by Kim et al. They showed that increasing the number ... Dickson ME, Sigmund CD (July 2006). "Genetic basis of hypertension: revisiting angiotensinogen". Hypertension. 48 (1): 14-20. ...
Angiotensinogen is also known as renin substrate. It is cleaved at the N-terminus by renin to result in angiotensin I, which ... Angiotensinogen is an α-2-globulin synthesized in the liver and is a precursor for angiotensin, but has also been indicated as ... Asp-Arg-Val-Tyr-Ile-His-Pro-Phe-His-Leu-Val-Ile-... Plasma angiotensinogen levels are increased by plasma corticosteroid, ... In mice with a full body deficit of angiotensinogen, the effects observed were low newborn survival rate, stunted body weight ...
"A redox switch in angiotensinogen modulates angiotensin release". Nature. 468 (7320): 108-11. Bibcode:2010Natur.468..108Z. doi: ...
... s bind to the active site of renin and inhibit the binding of renin to angiotensinogen, which is the rate- ... Renin is a circulating enzyme that acts on a circulating peptide, angiotensinogen. Renin cleaves the peptide at the Leu10-Val11 ... Renin is highly selective for its only naturally occurring substrate which is angiotensinogen, and the incidence of unwanted ... The first generation of renin inhibitors, such as H-142, were peptide analogues of angiotensinogen. However, these inhibitors ...
Role of angiotensinogen. Cell 71 : 169-180, 1992. Rousseau A., Michaud A., Chauvet M-T., Lenfant M. and Corvol P. The ... Role of angiotensinogen". Cell. 71 (1): 169-80. doi:10.1016/0092-8674(92)90275-H. PMID 1394429. S2CID 12142319. Dive, V.; ...
Outside the liver, angiotensinogen is picked up from the circulation or expressed locally in some tissues; with renin they form ... Plasma renin then carries out the conversion of angiotensinogen, released by the liver, to a decapeptide called angiotensin I. ... Renin cleaves a decapeptide from angiotensinogen, a globular protein. The decapeptide is known as angiotensin I. Angiotensin I ...
Renin then acts by converting angiotensinogen to angiotensin I; angiotensin converting enzyme (ACE) converts angiotensin I to ...
Renin converts angiotensinogen (inactive form) to angiotensin I (active form). Angiotensin I flows in the bloodstream until it ... Renin converts angiotensinogen to angiotensin I, which is converted by angiotensin converting enzyme to angiotensin II. ...
"Kinetic studies of rat renin and tonin on purified rat angiotensinogen". Canadian Journal of Biochemistry and Cell Biology. 62 ...
February 1999). "Angiotensinogen gene polymorphisms M235T/T174M: no excess transmission to hypertensive Chinese". Hypertension ... It performs this function by breaking down (hydrolysing) angiotensinogen, secreted from the liver, into the peptide angiotensin ... angiotensinogen and epithelial sodium channel". Hypertension. 33 (6): 1324-31. doi:10.1161/01.hyp.33.6.1324. PMID 10373210. ...
"Novel Mechanism of Blood Pressure Regulation By Foxo1-Mediated Transcriptional Control of Hepatic Angiotensinogen". ...
2005). "Finb, a multiple zinc finger protein, represses transcription of the human angiotensinogen gene". Int. J. Mol. Med. 13 ...
Ricardo SD, Franzoni DF, Roesener CD, Crisman JM, Diamond JR (May 2000). "Angiotensinogen and AT(1) antisense inhibition of ...
Renin, a proteolytic enzyme, cleaves angiotensinogen to angiotensin I, which is converted to angiotensin II. In the case of ...
"Effect of Renin-Angiotensin System Blockade on the Expression of the Angiotensinogen Gene and Induction of Hypertrophy in Rat ... "Effect of renin-angiotensin system blockade on the expression of the angiotensinogen gene and induction of hypertrophy in rat ... "RAS blockade decreases blood pressure and proteinuria in transgenic mice over-expressing rat angiotensinogen gene in the kidney ... "Reactive oxygen species blockade and action of insulin on expression of angiotensinogen gene in proximal tubular cells". ...
... endothiapepsin and its complex with an angiotensinogen fragment analogue, H-142". Biochemical Society Transactions. 13 (6): ...
It cleaves angiotensinogen to angiotensin I, which is in turn converted by angiotensin-converting enzyme (ACE) to angiotensin ... Binding to this pocket prevents the conversion of angiotensinogen to angiotensin I. Aliskiren is also available as combination ...
Under normal physiological conditions, the enzyme renin converts angiotensinogen to angiotensin I, which will then be converted ...
Renin converts the inactive angiotensinogen into angiotensin I, which is converted to angiotensin II (AII) by angiotensin ...
"Upregulation of immunoreactive angiotensin II release and angiotensinogen mRNA expression by high-frequency preganglionic ...
The deletion increased the vascular angiotensinogen gene expression in the aorta which activated the renin-angiotensin system ...
Juxtaglomerular cells secrete renin, which converts angiotensinogen to angiotensin I, which is then converted to angiotensin II ...
Binding of renin to this receptor induces the conversion of angiotensinogen to angiotensin I. This protein is associated with ...
... from a plasma α-2-globulin called angiotensinogen. This decapeptide is known as angiotensin I. It has no known biological ...
1995). "Identification of angiotensinogen and complement C3dg as novel proteins binding the proform of eosinophil major basic ... angiotensinogen (AGT), and C3dg. This protein may be involved in antiparasitic defense mechanisms as a cytotoxin and helmintho- ...
... participates in the control of body fluid homeostasis by regulating angiotensinogen gene transcription in the rat subfornical ...
It produces and secretes into the circulation the enzyme renin (angiotensinogenase), which cleaves angiotensinogen and results ...
Urine Angiotensinogen. AGT is a 453 amino acid-long protein cleaved by renin to form angiotensin 1. Increased urine AGT is a ... Urinary Angiotensinogen Level Predicts AKI in Acute Decompensated Heart Failure: A Prospective, Two-Stage Study. J Am Soc ...
Analysis of the angiotensinogen gene in the MRC British genetics of Hypertension study. ... Analysis of the angiotensinogen gene in the MRC British genetics of Hypertension study. ...
Control myocardial angiotensinogen was 0.042±0.004 μmol/kg myocardium and plasma angiotensinogen was 1.5 μmol/L plasma. Two ... Control myocardial angiotensinogen was 0.042±0.004 μmol/kg myocardium and plasma angiotensinogen was 1.5 μmol/L plasma. Two ... Control myocardial angiotensinogen was 0.042±0.004 μmol/kg myocardium and plasma angiotensinogen was 1.5 μmol/L plasma. Two ... Control myocardial angiotensinogen was 0.042±0.004 μmol/kg myocardium and plasma angiotensinogen was 1.5 μmol/L plasma. Two ...
AGT: angiotensinogen. *AGTR1: angiotensin II receptor type 1. *AGXT: alanine--glyoxylate aminotransferase ...
angiotensinogen. involved_in. IMP. PMID:8252633. BHF-UCL. PMID:8252633. RGD:8553951. NCBI chr19:52,529,139...52,549,618 Ensembl ...
"Interleukin-6 Mediates Angiotensinogen Gene Expression during Liver Regeneration". PLOS ONE. 8 (7): e67868. Bibcode:2013PLoSO ... Dzau, VJ; Herrmann, HC (15-22 February 1982). "Hormonal control of angiotensinogen production". Life Sciences. 30 (7-8): 577-84 ... Angiotensinogen expression Regenerate itself by hepatocyte mitosis Via STAT and Gab1: RAS/MAPK, PLC/IP3 and PI3K/FAK Cell ...
Urinary Angiotensinogen in addition to Imaging Classification in the Prediction of Renal Outcome in Autosomal Dominant ... Urinary Angiotensinogen in addition to Imaging Classification in the Prediction of Renal O ... Urinary angiotensinogen to creatinine ratio (AGT/Cr) was suggested as a novel biomarker to reflect intrarenal RAS activity. ...
Angiotensinogen Catalog No: 123-03 Form: Lyophilized 123-03. Human Plasma. > 95% (SDS-PAGE). Lyophilized. More Info. ...
Crystal structure of mouse angiotensinogen in the reduced form. 2wxz. Crystal structure of rat angiotensinogen in C2 space ... Crystal structure of rat angiotensinogen in P321 space group. 2x0b. Crystal structure of human angiotensinogen complexed with ... Angiotensinogen (P01019) (SMART). OMIM:106150: {Hypertension, essential, susceptibility to} ; {Preeclampsia, susceptibility to} ... Crystal structure of mouse angiotensinogen in the oxidised form. 2wxy. ...
We quantified circulating angiotensinogen and renin by enzyme-kinetic assay, tissue angiotensinogen by Western blotting, and ... Gene silencing of liver angiotensinogen using siRNA lowered circulating angiotensinogen by 97 ± 0.3%, and made brainstem ... angiotensin II, angiotensinogen, brain, mineralocorticoid receptor antagonism, RNAi therapeutics, salt-sensitive hypertension ... To this end, chronic DOCA-salt-hypertensive rats were treated with liver-directed siRNA targeted to angiotensinogen, the ...
Additionally, vitamin D analogs (such as paricalcitol) block angiotensinogen production and renin expression in renal cells ( ...
In July, The New England Journal published a study of zilebesiran, an siRNA that inhibits the production of angiotensinogen, to ... Similar story: One injection led to a basically complete suppression of angiotensinogen and a sustained decrease in blood ...
Renin breaks Angiotensinogen to Angiotensin I*Angiotensin Converting Enzyme (lungs and capillaries) converts Angiotensin I to ...
Adipose cells secrete leptin, resistin, adiponectin, adipsin, acylation-stimulating protein, angiotensinogen, tumour necrosis ...
Low expression of angiotensinogen and dipeptidyl peptidase 1 in saliva of patients with proliferative verrucous leukoplakia. ...
... and angiotensinogen correlated inversely with eGFR and were selected for the Cox regression. Mean follow-up was 5.2 years ... and angiotensinogen correlated inversely with eGFR and were selected for the Cox regression. Mean follow-up was 5.2 years ...
This system is a multi-enzymatic cascade in which angiotensinogen, the major substrate, is processed in a two-step reaction by ... Angiotensinogen Angiotensinogen, the substrate for renin, is the source of all angiotensin peptides. Angiotensinogen in the ... Angiotensinogen is cleaved by renin to form angiotensin I, which is then cleaved by angiotensin-converting enzyme (ACE) to form ... Along with angiotensinogen, the kidney expresses all of the other components of the RAS. Accordingly, it has been suggested ...
Renin, an enzyme produced in the kidney, acts on angiotensinogen, an alpha-2 globulin produced by the liver, forming ... Renin, an enzyme produced in the kidney, acts on angiotensinogen, an alpha-2 globulin produced by the liver, forming ... angiotensinogen; angiotensin converting enzyme; angiotensin i; angiotensin ii; and angiotensinase. ... angiotensinogen; angiotensin converting enzyme; angiotensin i; angiotensin ii; and angiotensinase. ...
C angiotensinogen polymorphism. European journal of preventive cardiology 2012 Apr 19 (2): 199-204. Hager Alfred, Bildau Judith ...
Renin splits angiotensinogen, a large protein that circulates in the bloodstream, into pieces. One piece is angiotensin I. ...
Kidney-specific enhancement of ANG II stimulates endogenous intrarenal angiotensinogen in gene-targeted mice. Nor are they as ...
Renin cleaves angiotensin (ANG) I from angiotensinogen, which is further cleaved to ANG II by ANG-converting enzyme. ANG II ...
Transgenic mice and rats bearing renin and extra copies of angiotensinogen genes revealed the importance of brain RAS. Cre-lox ...
Renin converts the angiotensinogen produced in the liver into angiotensin I, which is later converted in the lungs into ...
Prev:Angiotensinogen M235T gene variants and its association with essential hypertension and plasma renin activity in Malaysian ...
Short-term Effects of Garlic-Based Diets on mRNA Expression of Angiotensinogen, Angiotensin-1 Converting Enzyme, and Atrial ... Statistics for Short-term Effects of Garlic-Based Diets on mRNA Expression of Angiotensinogen, Angiotensin-1 Converting Enzyme ...
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In the blood, renin initiates chemical reactions that convert a plasma protein, called angiotensinogen to a peptide, called ...
  • In an attempt to clarify the relationship of the circulating and myocardial renin-angiotensin systems, active renin concentration, its constituent major glycoforms (active renin glycoforms I through V), and angiotensinogen were measured in plasma and left ventricular homogenates from sodium-depleted rats under control conditions or 2 minutes, 3 hours, 6 hours, and 48 hours after bilateral nephrectomy (BNX). (umn.edu)
  • Forty-eight hours after BNX, myocardial renin concentrations had fallen to 15% of control values, while myocardial anglotensinogen concentrations had increased 12- fold and plasma angiotensinogen concentrations had increased by only 3.5- fold. (umn.edu)
  • RESULTS: Tissue factor, proteinase-activated receptor, soluble urokinase plasminogen activator surface receptor (suPAR), thrombomodulin, adrenomedullin, renin, and angiotensinogen correlated inversely with eGFR and were selected for the Cox regression. (lu.se)
  • This system is a multi-enzymatic cascade in which angiotensinogen, the major substrate, is processed in a two-step reaction by renin and angiotensin-converting enzyme (ACE), resulting in the sequential generation of angiotensins I and II. (abdominalkey.com)
  • Active renin specifically cleaves the 10 amino acids from the N-terminus of angiotensinogen to form angiotensin I. A substantial excess of angiotensinogen is present in serum, and ACE is ubiquitous in the endothelium and plasma. (abdominalkey.com)
  • Renin cleaves angiotensin (ANG) I from angiotensinogen, which is further cleaved to ANG II by ANG-converting enzyme. (imrpress.com)
  • Renin converts the angiotensinogen produced in the liver into angiotensin I, which is later converted in the lungs into angiotensin II. (flkidney.com)
  • Angiotensinogen M235T gene variants and its association with essential hypertension and plasma renin activity in Malaysian subject - A case control study. (grmrc.org)
  • During the current period, we demonstrated that deficiency of adipocyte-derived angiotensinogen (AGT) prevented elevations in adipose and systemic angiotensin II (AngII) concentrations and abolished the development of hypertension in obese male mice. (uky.edu)
  • Analysis of the angiotensinogen gene in the MRC British genetics of Hypertension study. (ox.ac.uk)
  • Urinary Angiotensinogen in addition to Imaging Classification in the Prediction of Renal Outcome in Autosomal Dominant Polycystic Kidney Disease. (bvsalud.org)
  • This peptide is a renin substrate (angiotensinogen) labeled with EDANS/ DABCYL FRET pair for renin activity studies. (eurogentec.com)
  • The enzymatic cascade by which angiotensin II is produced consists of renin, which cleaves angiotensinogen to form the decapeptide angiotensin-I. Angiotensin-I is then further cleaved by angiotensin-converting enzyme (ACE) to produce angiotensin II, the physiologically active component of the system. (vin.com)
  • 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. (bvsalud.org)
  • angiotensinogen) The protein encoded by this gene, pre-angiotensinogen or angiotensinogen precursor, is expressed in the liver and is cleaved by the enzyme renin in response to lowered blood pressure. (genebe.net)
  • C angiotensinogen polymorphism. (cdc.gov)
  • Genetic Association of Angiotensinogen (M235T) Gene Polymorphism with Essential Hypertension in Vindhyan Population of Madhya Pradesh, India. (crdeepjournal.org)