A highly specific (Leu-Leu) endopeptidase that generates ANGIOTENSIN I from its precursor ANGIOTENSINOGEN, leading to a cascade of reactions which elevate BLOOD PRESSURE and increase sodium retention by the kidney in the RENIN-ANGIOTENSIN SYSTEM. The enzyme was formerly listed as EC 3.4.99.19.
A BLOOD PRESSURE regulating system of interacting components that include RENIN; ANGIOTENSINOGEN; ANGIOTENSIN CONVERTING ENZYME; ANGIOTENSIN I; ANGIOTENSIN II; and angiotensinase. Renin, an enzyme produced in the kidney, acts on angiotensinogen, an alpha-2 globulin produced by the liver, forming ANGIOTENSIN I. Angiotensin-converting enzyme, contained in the lung, acts on angiotensin I in the plasma converting it to ANGIOTENSIN II, an extremely powerful vasoconstrictor. Angiotensin II causes contraction of the arteriolar and renal VASCULAR SMOOTH MUSCLE, leading to retention of salt and water in the KIDNEY and increased arterial blood pressure. In addition, angiotensin II stimulates the release of ALDOSTERONE from the ADRENAL CORTEX, which in turn also increases salt and water retention in the kidney. Angiotensin-converting enzyme also breaks down BRADYKININ, a powerful vasodilator and component of the KALLIKREIN-KININ SYSTEM.
An alpha-globulin of about 453 amino acids, depending on the species. It is produced by the liver and secreted into blood circulation. Angiotensinogen is the inactive precursor of natural angiotensins. Upon successive enzyme cleavages, angiotensinogen yields angiotensin I, II, and III with amino acids numbered at 10, 8, and 7, respectively.
A hormone secreted by the ADRENAL CORTEX that regulates electrolyte and water balance by increasing the renal retention of sodium and the excretion of potassium.
Body organ that filters blood for the secretion of URINE and that regulates ion concentrations.
Compounds based on fumaric acid.
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.
PRESSURE of the BLOOD on the ARTERIES and other BLOOD VESSELS.
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.
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 benzoic-sulfonamide-furan. It is a diuretic with fast onset and short duration that is used for EDEMA and chronic RENAL INSUFFICIENCY.
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.
Physiologically inactive substances that can be converted to active enzymes.
A diet which contains very little sodium chloride. It is prescribed by some for hypertension and for edematous states. (Dorland, 27th ed)
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.
Organic compounds containing the -CO-NH2 radical. Amides are derived from acids by replacement of -OH by -NH2 or from ammonia by the replacement of H by an acyl group. (From Grant & Hackh's Chemical Dictionary, 5th ed)
Persistent high BLOOD PRESSURE due to KIDNEY DISEASES, such as those involving the renal parenchyma, the renal vasculature, or tumors that secrete RENIN.
Hypertension due to RENAL ARTERY OBSTRUCTION or compression.
A member of the alkali group of metals. It has the atomic symbol Na, atomic number 11, and atomic weight 23.
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 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.
One of two salivary glands in the neck, located in the space bound by the two bellies of the digastric muscle and the angle of the mandible. It discharges through the submandibular duct. The secretory units are predominantly serous although a few mucous alveoli, some with serous demilunes, occur. (Stedman, 25th ed)
Drugs used in the treatment of acute or chronic vascular HYPERTENSION regardless of pharmacological mechanism. Among the antihypertensive agents are DIURETICS; (especially DIURETICS, THIAZIDE); ADRENERGIC BETA-ANTAGONISTS; ADRENERGIC ALPHA-ANTAGONISTS; ANGIOTENSIN-CONVERTING ENZYME INHIBITORS; CALCIUM CHANNEL BLOCKERS; GANGLIONIC BLOCKERS; and VASODILATOR AGENTS.
Excision of kidney.
The circulation of the BLOOD through the vessels of the KIDNEY.
A condition of markedly elevated BLOOD PRESSURE with DIASTOLIC PRESSURE usually greater than 120 mm Hg. Malignant hypertension is characterized by widespread vascular damage, PAPILLEDEMA, retinopathy, HYPERTENSIVE ENCEPHALOPATHY, and renal dysfunction.
The amount of a substance secreted by cells or by a specific organ or organism over a given period of time; usually applies to those substances which are formed by glandular tissues and are released by them into biological fluids, e.g., secretory rate of corticosteroids by the adrenal cortex, secretory rate of gastric acid by the gastric mucosa.
An antagonist of ANGIOTENSIN TYPE 1 RECEPTOR with antihypertensive activity due to the reduced pressor effect of ANGIOTENSIN II.
Works containing information articles on subjects in every field of knowledge, usually arranged in alphabetical order, or a similar work limited to a special field or subject. (From The ALA Glossary of Library and Information Science, 1983)
Messages between computer users via COMPUTER COMMUNICATION NETWORKS. This feature duplicates most of the features of paper mail, such as forwarding, multiple copies, and attachments of images and other file types, but with a speed advantage. The term also refers to an individual message sent in this way.
Mechanical food dispensing machines.
The guidelines and policy statements set forth by the editor(s) or editorial board of a publication.
The profession of writing. Also the identity of the writer as the creator of a literary production.
A publication issued at stated, more or less regular, intervals.
The functions and activities carried out by the U.S. Postal Service, foreign postal services, and private postal services such as Federal Express.
A loose confederation of computer communication networks around the world. The networks that make up the Internet are connected through several backbone networks. The Internet grew out of the US Government ARPAnet project and was designed to facilitate information exchange.
Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.
An analog of desoxycorticosterone which is substituted by a hydroxyl group at the C-18 position.
A group of CORTICOSTEROIDS primarily associated with water and electrolyte balance. This is accomplished through the effect on ION TRANSPORT in renal tubules, resulting in retention of sodium and loss of potassium. Mineralocorticoid secretion is itself regulated by PLASMA VOLUME, serum potassium, and ANGIOTENSIN II.
A mitochondrial cytochrome P450 enzyme that catalyzes the 18-hydroxylation of steroids in the presence of molecular oxygen and NADPH-specific flavoprotein. This enzyme, encoded by CYP11B2 gene, is important in the conversion of CORTICOSTERONE to 18-hydroxycorticosterone and the subsequent conversion to ALDOSTERONE.
Techniques for measuring blood pressure.
Method in which repeated blood pressure readings are made while the patient undergoes normal daily activities. It allows quantitative analysis of the high blood pressure load over time, can help distinguish between types of HYPERTENSION, and can assess the effectiveness of antihypertensive therapy.
Increased VASCULAR RESISTANCE in the PULMONARY CIRCULATION, usually secondary to HEART DISEASES or LUNG DISEASES.
Time period from 1801 through 1900 of the common era.

Effects of long-term administration of clonidine on plasma renin activity. (1/3749)

Plasma renin activity (PRA) was studied before and during long-term treatment with moderate oral doses (0.2 or 0.3 mg/d) of clonidine. Nine outpatients with essential hypertension received clonidine for 12 weeks; a significant decrease in blood pressure was evident in all patients. Except for a nonsignificant increase after 12 weeks of treatment, PRA values were not notably changed by clonidine therapy. No correlation was found between individual blood pressure changes and PRA variation during the study. The absence of a net effect on PRA in this study does not exclude more complex interactions of clonidine with the renin-angiotensin system. Nonetheless, clonidine cannot generally be classified as a "renin-inhibiting" drug.  (+info)

Intrarenal site of action of calcium on renin secretion in dogs. (2/3749)

We studied the effects of intrarenal calcium infusion on renin secretion in sodium-depleted dogs in an attempt to elucidate the major site of calcium-induced inhibition of renin release. Both calcium chloride and calcium gluconate reduced renal blood flow and renin secretion while renal perfusion pressure was unchanged. These data indicate that calcium inhibition of renin secretion did not occur primarily at the renal vascular receptor; decreased renal blood flow is usually associated with increased renin secretion. Calcium chloride infusion increased urinary chloride excretion without affecting sodium excretion, and calcium gluconate failed to increase either sodium or chloride excretion. Also, the filtered loads of sodium and chloride were unchanged during the calcium infusions. These results give no indication that calcium inhibited renin secretion by increasing the sodium or chloride load at the macula densa. The effects of intrarenal calcium infusion on renin release were also assessed in dogs with a nonfiltering kidney in which renal tubular mechanisms could not influence renin secretion. The observation that calcium still suppressed renin release in these dogs provides additional evidence that the the major effect of calcium involved nontubular mechanisms. Thus, it appears likely that calcium acted directly on the juxtaglomerular cells to inhibit renin secretion.  (+info)

Stimulation of renin release from rabbit renal cortex by arachidonic acid and prostaglandin endoperoxides. (3/3749)

The mechanism by which renal prostaglandins stimulate renin secretion in vivo is unknown. In this in vitro study we measured the effects of activation of the prostaglandin (PG) system on renin release from slices of rabbit renal cortex. The PG precursor arachidonic acid (C20:4), a natural PG endoperoxide (PGG2), two stable synthetic PG endoperoxide analogues (EPA I and II), PGE2, PGF2alpha, and two different PG synthesis inhibitors [indomethacin and 5,8,11,14-eicosatetraynoic acid (ETA)] were used to evaluate the possibility of a direct action of the cortical PG system on renin secretion. Renin release increased significantly with time after addition of C20:4, PGG2, EPA I, and EPA II to the incubation medium. Stimulation of renin release was se-related for C20:4 in concentrations of 0.6 to 4.5 X 10(-6) M, for EPA I in concentrations of 0.7 to 2.8 X 10(-6) M, and for EPA II in concentrations of 1.4 to 14.0 X 10(-6) M. Indomethacin (10(-4) M) and ETA (10(-4) M) significantly decreased basal renin release as well as the renin release stimulated by C20:4 and EPA I. PGE2(10(-12) to 10(-6) M) had no effect on renin release, whereas PGF2alpha (10(-12) to 10(-6) M) decreased renin release in a dose-dependent manner. These data raise the possibility of a direct action of the renal cortical PG system on renin secretion. The results further indicate that stimulation of renin release by C20:4 may depend more specifically on the action of PG endoperoxides than on the primary prostaglandins.  (+info)

An alternative transcript of the rat renin gene can result in a truncated prorenin that is transported into adrenal mitochondria. (4/3749)

Characterization of the local renin-angiotensin system in the rat adrenal zona glomerulosa indicated a dual targeting of renin both to the secretory pathway and mitochondria. To investigate the transport of renin into mitochondria, we constructed a series of amino-terminal deletion variants of preprorenin. One of these variants, lacking the complete signal sequence for the endoplasmic reticulum and 10 amino acids of the profragment, was transported efficiently into isolated mitochondria. The transport was further shown to be dependent on mitochondrial membrane potential and ATP synthesis. Analysis of adrenal RNA revealed the existence of 2 renin transcripts. While one of the transcripts corresponds to the known full-length transcript, the other one lacks exon 1; instead, exon 2 is preceded by a domain of 80 nucleotides originating from intron 1. This domain, as well as the following region of intron 1 being excised, shows all essential sequence elements defining an additional, so-far-unknown exon. The second mRNA possibly derives from an additional transcription start in intron 1 and an alternative splicing process. Translation of this mRNA could result in a truncated prorenin representing a cytosolic form of renin, which is required for transport into mitochondria. This truncated prorenin corresponds exactly to the deletion variant being imported into mitochondria in vitro.  (+info)

Low calorie diet enhances renal, hemodynamic, and humoral effects of exogenous atrial natriuretic peptide in obese hypertensives. (5/3749)

The expression of the natriuretic peptide clearance receptor is abundant in human and rat adipose tissue, where it is specifically inhibited by fasting. In obese hypertensives, plasma atrial natriuretic peptide (ANP) levels were found to be lower than in obese normotensives. Therefore, the increased adipose mass might influence ANP levels and/or its biological activity. The aim of the present study was to evaluate whether the humoral, hemodynamic, and renal effects of exogenous ANP in obese hypertensives might be enhanced by a very low calorie diet. Eight obese hypertensives received a bolus injection of ANP (0.6 mg/kg) after 2 weeks of a normal calorie/normal sodium diet, and blood pressure (BP), heart rate, ANP, cGMP, plasma renin activity, and aldosterone were evaluated for 2 hours before and after the injection. Diuresis and natriuresis were measured every 30 minutes. The patients then started a low calorie/normal sodium diet (510 kcal/150 mmol/d) for 4 days, and then the ANP injection protocol was repeated. The low calorie diet induced a slight weight loss (from 90.6+/-1.1 to 87. 7+/-1.2 kg; P<0.01), which was accompanied by increase of cGMP excretion (from 146.0+/-10.1 to 154.5+/-9.5 nmol/24 h; P<0.05) together with a reduction of BP (P<0.01 versus basal levels). ANP injection after diet was followed by an increase of ANP levels similar to that observed before diet, but plasma cGMP, diuresis, and natriuresis increased significantly only after diet. Similarly, the decrease of BP after ANP administration was significantly higher after diet (change in mean arterial pressure, -6.4+/-0.7 versus -4. 0+/-0.6 mm Hg; P<0.05) as well as that of aldosterone (P<0.01). These data show that a low calorie diet enhances the humoral, renal, and hemodynamic effects of ANP in obese hypertensives and confirm the importance of caloric intake in modulating the biological activity of ANP, suggesting that the natriuretic peptide system can play a role in the acute changes of natriuresis and diuresis associated with caloric restriction.  (+info)

Recovery following relief of unilateral ureteral obstruction in the neonatal rat. (6/3749)

BACKGROUND: Obstructive nephropathy is a primary cause of renal insufficiency in infants and children. This study was designed to distinguish the reversible and irreversible cellular consequences of temporary unilateral ureteral obstruction (UUO) on the developing kidney. METHODS: Rats were subjected to UUO or sham operation in the first 48 hours of life, and the obstruction was removed five days later (or was left in place). Kidneys were removed for study 14 or 28 days later. In additional groups, kidneys were removed at the end of five days of obstruction. Immunoreactive distribution of renin was determined in arterioles, and the distribution of epidermal growth factor, transforming growth factor-beta1, clusterin, vimentin, and alpha-smooth muscle actin was determined in tubules and/or interstitium. The number of glomeruli, glomerular maturation, tubular atrophy, and interstitial collagen deposition was determined by morphometry. Renal cellular proliferation and apoptosis were measured by proliferating cell nuclear antigen and the TdT uridine-nick-end-label technique, respectively. The glomerular filtration rate was measured by inulin clearance. RESULTS: Renal microvascular renin maintained a fetal distribution with persistent UUO; this was partially reversed by the relief of obstruction. Although glomerular maturation was also delayed and glomerular volume was reduced by UUO, the relief of obstruction prevented the reduction in glomerular volume. Although relief of obstruction did not reverse a 40% reduction in the number of nephrons, the glomerular filtration rate of the postobstructed kidney was normal. The relief of obstruction did not improve tubular cell proliferation and only partially reduced apoptosis induced by UUO. This was associated with a persistent reduction in the tubular epidermal growth factor. In addition, the relief of obstruction reduced but did not normalize tubular expression of transforming growth factor-beta1, clusterin, and vimentin, all of which are evidence of persistent tubular injury. The relief of obstruction significantly reduced interstitial fibrosis and expression of alpha-smooth muscle actin by interstitial fibroblasts, but not to normal levels. CONCLUSIONS: The relief of obstruction in the neonatal rat attenuates, but does not reverse, renal vascular, glomerular, tubular, and interstitial injury resulting from five days of UUO. Hyperfiltration by remaining nephrons and residual tubulointerstitial injury in the postobstructed kidney are likely to lead to deterioration of renal function later in life.  (+info)

Long-term effects of growth hormone (GH) on body fluid distribution in GH deficient adults: a four months double blind placebo controlled trial. (7/3749)

OBJECTIVE: Short-term growth hormone (GH) treatment normalises body fluid distribution in adult GH deficient patients, but the impact of long-term treatment on body fluid homeostasis has hitherto not been thoroughly examined in placebo controlled trials. To investigate if the water retaining effect of GH persists for a longer time we examined the impact of 4 months GH treatment on extracellular volume (ECV) and plasma volume (PV) in GH deficient adults. DESIGN: Twenty-four (18 male, 6 female) adult GH deficient patients aged 25-64 years were included and received either GH (n=11) or placebo (n=13) in a double blind parallel design. METHODS: Before and at the end of each 4 month period ECV and PV were assessed directly using 82Br- and 125I-albumin respectively, and blood samples were obtained. RESULTS: During GH treatment ECV increased significantly (before: 20.48+/-0.99 l, 4 months: 23.77+/-1.38 l (P<0.01)), but remained unchanged during placebo administration (before: 16.92+/-1.01 l, 4 months: 17.60+/-1.24 l (P=0.37)). The difference between the groups was significant (P<0.05). GH treatment also increased PV (before: 3.39+/-0.27 l. 4 months: 3.71+/-0.261 (P=0.01)), although an insignificant increase in the placebo treated patients (before: 2.81+/-0.18 l, 4 months: 2.89+/-0.20 l (P=0.37)) resulted in an insignificant treatment effect (P=0.07). Serum insulin-like growth factor-I increased significantly during GH treatment and was not affected by placebo treatment. Plasma renin (mIU/l) increased during GH administration (before: 14.73+/-2.16, 4 months: 26.00+/-6.22 (P=0.03)) and remained unchanged following placebo (before: 20.77+/-5.13, 4 months: 20.69+/-6.67 (P=0.99)) leaving no significant treatment effect (P=0.08). CONCLUSION: The long-term impact of GH treatment on body fluid distribution in adult GH deficient patients involves expansion of ECV and probably also PV. These data substantiate the role of GH as a regulator of fluid homeostasis in adult GH deficiency.  (+info)

Tranilast suppresses vascular chymase expression and neointima formation in balloon-injured dog carotid artery. (8/3749)

BACKGROUND: Activation of vascular chymase plays a major role in myointimal hypertrophy after vascular injury by augmenting the production of angiotensin (ANG) II. Because chymase is synthesized mainly in mast cells, we assumed that the chymase-dependent ANG II formation could be downregulated by tranilast, a mast cell-stabilizing antiallergic agent. We have assessed inhibitory effects of tranilast on neointima formation after balloon injury in the carotid artery of dogs, which share a similar ANG II-forming chymase with humans, and further explored the pathophysiological significance of vascular chymase. METHODS AND RESULTS: Either tranilast (50 mg/kg BID) or vehicle was orally administered to beagles for 2 weeks before and 4 weeks after balloon injury. Four weeks after the injury, remarkable neointima was formed in the carotid arteries of vehicle-treated dogs. Chymase mRNA levels and chymaselike activity of vehicle-treated injured arteries were increased 10.2- and 4.8-fold, respectively, those of uninjured arteries. Angiotensin-converting enzyme (ACE) activity was slightly increased in the injured arteries, whereas ACE mRNA levels were not. Tranilast treatment completely prevented the increase in chymaselike activity, reduced the chymase mRNA levels by 43%, and decreased the carotid intima/media ratio by 63%. In vehicle-treated injured arteries, mast cell count in the adventitia showed a great increase, which was completely prevented by the tranilast treatment. Vascular ACE activity and mRNA levels were unaffected by tranilast. CONCLUSIONS: Tranilast suppressed chymase gene expression, which was specifically activated in the injured arteries, and prevented neointima formation. Suppression of the chymase-dependent ANG II-forming pathway may contribute to the beneficial effects of tranilast.  (+info)

In this study, we provide experimental evidence in favor of the hypothesis that PPARs are involved in the control of renin gene expression. We predicted a role for PPARs in the regulation of renin gene expression using a molecular approach. There was strong initial evidence supporting such a role.7,12 A functional DNA-binding site, similar to the consensus motif for PPARs, was detected in the conserved 5′-renin gene enhancer. The retinoic acid nuclear receptor RXRα, which is the typical interaction partner for PPARs, binds to the mouse renin gene enhancer. Lastly, vitamin A, which is the natural ligand of RXRs, was found to stimulate the transcription of the renin gene.. Renin gene expression is upregulated by cAMP in CaLu-6 cells through stabilization of renin mRNA, although transcriptional mechanisms are also involved.17,21 We provided several lines of evidence that PPARγ stimulates renin gene expression without affecting the stability of renin mRNA (Figures 1, 2, and 5⇑⇑; data not ...
We studied the source of inactive renin in plasma by investigating the changes of active and inactive renin after bilateral nephrectomy in the rat. Active renin rapidly decreased after bilateral nephrectomy, with a half-life of approximately 15 minutes. Inactive renin, on the other hand, was 20.96 +/- 1.63 ng/ml/hr before nephrectomy and gradually increased to reach a peak at 20 hours after nephrectomy (193 +/- 62 ng/ml/hr). The molecular weight of active renin was approximately 40,000 and that of inactive renin was approximately 60,000 on a Sephacryl S-200 column. Inactive renin was separated from active renin by a Cibacron blue column, and the 0 time inactive renin eluted in the same fractions as the inactive renin from 20 hours after nephrectomy. The pH optimum of inactive renin in rat renin substrate was between 5.5 and 7.5, which differs from the optimal value of pepsin or cathepsin D. The increase of inactive renin in nephrectomized rats was not prevented by removal of the salivary glands, ...
The response of renin release to the administration of renin inhibitors cannot be studied with conventional enzymatic methods used to measure plasma renin. In the present experiments, a novel multirange enzyme-linked immunosorbent assay for human and primate renin was used to investigate the changes in plasma immunoreactive renin after renin inhibition. A potent and long-acting statine-containing renin inhibitor, CGP 29 287, was injected in conscious marmosets after mild or severe sodium depletion. In mildly sodium-depleted marmosets, CGP 29 287 (0.1 mg/kg i.v.) reduced mean arterial blood pressure and completely inhibited plasma renin activity for up to 30 minutes. This response was associated with a transient increase in plasma immunoreactive renin concentration. After a dose of 1.0 mg/kg i.v., the reduction of mean arterial pressure and the complete inhibition of plasma renin activity persisted for up to 120 minutes. These effects were accompanied by a sustained increase in plasma ...
TY - JOUR. T1 - Active and Inactive Renin after SQ 14225 (Captopril) Administration. AU - Goto, Toshikazu. AU - Abe, Keishi. AU - Otsuka, Yoichi. AU - Itoh, Toru. AU - Imai, Yutaka. AU - Satoh, Makito. AU - Omata, Ken. AU - Yoshinaga, Kaoru. PY - 1980/1/1. Y1 - 1980/1/1. N2 - The changes of active and inactive renin in plasma after the oral administration of 25 mg or 50 mg of SQ 14225 (Captopril) were studied in 29 hypertensive patients. Inactive renin was calculated as plasma renin activity (PRA) after cold storage minus PRA before cold storage. The patients were divided into 2 groups, responders and non-responders, according to the response of active renin to Captopril. In 9 responders, the active renin increased markedly while the inactive renin decreased. On the other hand, in 20 non-responders, both renin activities increased only slightly. These results suggest that inactive renin may be converted in vivo to active renin by Captopril.. AB - The changes of active and inactive renin in ...
TY - JOUR. T1 - Aortic endothelial cell activity in high renin and normal renin models of hypertension in the rat. AU - Daniel, R. E.. AU - Boitnott, J. K.. AU - Brown, G. D.. AU - Heptinstall, R. H.. PY - 1982/12/1. Y1 - 1982/12/1. N2 - To determine whether renin or angiotensin might have an effect on endothelial cell activity, we studied cell replication and cell density in two models of hypertension in the rat. The first was a model in which the plasma renin activity was high during the three time periods studied (1, 2, and 4 weeks after renal artery constriction) and the second, a model with elevated plasma renin activity only during the initial period (1 week). Aortic endothelial cells were labeled with tritiated thymidine prior to killing, and en face endothelial cell monolayers were prepared. The ratio of labeled cells to total cells (thymidine index) and the ratio of total number of cells to number of fields observed (cell density) were calculated for the whole aorta, segments of the ...
Assay Kits , Renin Assay Kits , SensoLyte ® 520 Mouse Renin Assay Kit *Fluorimetric*; Renin, a highly specific aspartyl protease, cleaves angiotensinogen, to yield angiotensin I. Angiotensin I is further converted into angiotensin II by ACE (Angiotensin Converting Enzyme). Angiotensin II constricts blood vessels leading to increased blood pressure. Discovery of new renin inhibitors for treatment of hypertension is a promising area of research. The SensoLyte 520 Mouse Renin Assay Kit provides a convenient assay for high throughput screening of renin inhibitors and for continuous assay of mouse renin activity using a 5-FAM/QXL 520 FRET peptide. In the FRET peptide the fluorescence of 5-FAM is quenched by QXL 520. Upon cleavage into two separate fragments by renin, the fluorescence of 5-FAM is recovered, and can be monitored at excitation/emission = 490/520 nm. The kit contains: 5-FAM/QXL 520-based FRET mouse specific renin substrate (Ex/Em=490/520 nm upon cleavage),
A gene-drug interaction has been indicated between beta-1 selective beta-blockers and the Arg389Gly polymorphism (rs1801253) in the adrenergic beta-1 receptor gene (ADRB1). We studied the effect of the ADRB1 Arg389Gly polymorphism on plasma renin activity (PRA) and heart rate (HR) and the genotype-dependent response to metoprolol and exercise. Twenty-nine healthy male subjects participated in 2 treatment periods (placebo and metoprolol). A 15-min submaximal exercise test was performed after each treatment period, and PRA and HR were measured before and after exercise. Before exercise, median PRA was lower in Gly/Gly subjects than in Arg/Arg subjects after both placebo (P = 0.030) and metoprolol treatment (P = 0.020). After placebo, the exercise-induced PRA increase was greater in Gly/Gly than in Arg/Gly and Arg/Arg subjects (P = 0.033). The linear association between log(PRA) and log(metoprolol concentration) varied significantly between genotypes (P = 0.024). In Gly/Gly subjects, PRA decreased ...
The primary structure of human renin precursor has been deduced from its cDNA sequence. A library of cDNA clones was constructed from human kidney poly(A)+ RNA by applying the vector/primer method of Okayama and Berg. The library was screened for human renin sequences by hybridization with the previously cloned mouse renin cDNA. Of the 240,000 colonies screened, 35 colonies that were positive for hybridization were isolated. Two recombinant plasmids containing long inserts of about 1,300 and 1,600 base pairs were selected for sequence analysis. The amino acid sequence predicted from the cDNA sequence shows that the human renin precursor consists of 406 amino acids with a pre and a pro segment carrying 20 and 46 amino acids, respectively. A high degree of sequence homology was found upon comparison of the mouse and human renins. Close similarities were also observed in the primary structures of renin and aspartyl proteinases that have known three-dimensional structures, suggesting a similar ...
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1. Blood pressure, heart rate and changes of plasma renin concentration (PRC) have been studied in nineteen patients with traumatic transection of the spinal cord, in relation to change of posture from supine to upright.. 2. When supine, subjects with cervical-cord transection had a normal blood pressure, a low heart rate and a high plasma renin concentration. On change of posture to the vertical, orthostatic hypotension developed, heart rate rose and PRC increased. Orthostatic hypotension was not a feature with change of posture in patients with transection of the thoracic spinal cord and PRC rose to a much smaller extent.. 3. It is concluded that release of renin on change of posture can occur in patients with spinal-cord transection. Release of renin in man does not depend therefore upon an intact autonomic nervous system, though it is possible that reflex sympathetic pathways in the isolated spinal cord may be involved. ...
The cardiovascular effects of vitamin D therapy (in humans) have been documented only in patients with known vitamin D deficiency or hyperparathyroidism (a surrogate marker of inadequate vitamin D activity). It is unknown whether the cardiovascular benefits of vitamin D therapy extend beyond these patients to the general hypertensive population. We propose to directly measure the effect of vitamin D therapy on plasma renin activity (PRA), plasma renin concentration (PRC), renin transcription (in mononuclear leukocytes), and blood pressure in hypertensive (but otherwise healthy) patients in a randomized, controlled, experimental trial. This will be the first study to assess vitamin D receptor (VDR) biological (PRA, PRC, renin mRNA, and polymorphisms) and hypertensive activity in patients without vitamin D deficiency. We hypothesize that vitamin D inhibition of renin transcription will produce significant reductions in PRA, PRC, renin transcription, inflammatory cytokines, SBP, and DBP, with ...
The Renin-Angiotensin System (RAS) is crucial in the regulation of the blood pressure (BP). Synthesis and secretion of Renin is the key regulated event in the operation of the RAS. One of the main mechanisms that control Renin synthesis and release is the baroreceptor mechanism whereby a decrease in BP results in increased release of Renin by juxtaglomerular (JG) Cells. Under normal circumstances, secretion of Renin by JG cells is sufficient to balance transient changes in BP. However, if the drop in renal perfusion pressure is protracted, additional Cells along the renal arterioles are transformed to the Renin phenotype to meet the perceived demands for Renin and regain homeostasis. In spite of its enormous importance, the nature and location of the renal baroreceptor, and whether mechanical signals are transmitted directly to the Renin cell nucleus to activate Renin gene expression is still unknown. It has been assumed that this pressure sensing mechanism is located at the afferent arterioles ...
The aspartyl-protease renin is the key regulator of the renin-angiotensin-aldosterone system, which is critically involved in extracellular fluid volume and blood pressure homeostasis of the body. Renin is synthesized, stored in, and released into circulation by the juxtaglomerular (JG) cells of the kidney. Secretion of renin from JG cells at the organ level is controlled by the four main mechanisms: the sympathetic nervous system, the local JG apparatus baroreflex, the macula densa mechanism, and several hormones acting locally within the JG apparatus. Renin secretion at the level of renal JG cells appears to be controlled mainly by classic second messengers, namely cAMP, cGMP, and free cytosolic calcium concentration. While cAMP generally stimulates renin release and the intracellular calcium concentration suppresses the exocytosis of renin, the effects of cGMP in the regulation of the renin system are more complex as it both may stimulate or inhibit renin release ...
The nonfiltering kidney model was used to determine whether sodium or potassium inhibits renin secretion in the absence of a functional macula densa in dogs with thoracic inferior vena caval constriction. The control rate of renin secretion was high, and decreases were readily recognized. After control observations, hypertonic sodium chloride or hypertonic potassium chloride was infused into the renal artery for 1 hour, and renin secretion was measured at 15-minute intervals. An increase in renal venous plasma sodium concentration from 141 to 154-158 mEq/liter caused no change in renin secretion for the first 45 minutes of infusion in dogs with a nonfiltering kidney. In contrast, dogs with thoracic caval constriction but with a filtering kidney showed a striking decrease in renin secretion during intrarenal sodium infusion (3,097 to 1,061 ng angiotensin/min, P ,0.02). An increase in renal venous plasma potassium concentration from 3.9 to 6.1 mEq/liter in one group of dogs and from 4.9 to 8.3 ...
1. The effects of infusions of equimolar doses of angiotensin II (AII) and of Des1-angiotensin II (heptapeptide) on plasma renin activity, blood pressure and plasma aldosterone were compared in normal anaesthetized dexamethasone-suppressed dogs.. 2. Plasma renin activity was equally suppressed by both compounds. The increase in blood pressure induced by the heptapeptide averaged 43-62% of the increase during AII infusions. No significant differences in aldosterone increase were observed between AII and the heptapeptide. Plasma aldosterone, however, dropped significantly faster in heptapeptide-treated dogs after the end of the infusions.. 3. Sar1-Ala8-angiotensin II (saralasin, 400 pmol min-1 kg-1) suppressed plasma aldosterone that was stimulated by heptapeptide (20 pmol min-1 kg-1) completely. The same angiotensin antagonist had only a moderate effect on plasma aldosterone stimulated by AII. After stopping the antagonist infusion, plasma aldosterone rose significantly higher in dogs infused ...
Renin is regulated by angiotensin subtype 1 (AT1) receptor, but it is unknown whether angiotensin subtype 2 (AT2) receptor contributes to this regulation. We hypothesized that AT2 receptors inhibit angiotensin II (Ang II) through inhibition of renin biosynthesis. We monitored changes in renal Ang II, renin mRNA and protein expression, and plasma renin concentration (PRC) in response to renal cortical administration of the AT1 receptor blocker valsartan or the AT2 receptor blocker PD 123319 (PD) in conscious rats administered low sodium intake (LS). Renal interstitial Ang II increased by 47-fold in response to LS and increased further in response to valsartan or PD by 67-fold and 61-fold from normal sodium diet (NS) and by 41% and 29% from LS, respectively. Renin mRNA increased 63% during LS, and either valsartan or PD increased it further by 600% and 250% from NS and 538% and 187% from LS, respectively. Similarly, renal renin content and PRC increased in response to LS and increased further in response
A method is described for estimating plasma renin activity by using renin substrate present in plasma. This method differs from other indirect renin assay methods by (1) incubation in the absence of ions thus establishing conditions for zero order kinetics for the reaction between endogeneous renin and substrate and (2) the use of angiotensinase inhibitors di-sodium ethylenediamine tetraacetic acid (EDTA) and d-isopropylfluorophosphate (DFP). Recoveries of renin added to plasma in levels similar to those occurring in plasma are 85% SD±7%.. The incubation was done at pH 5.5 which was shown to be the optimum for human renin reacting with human substrate.. By incubating human plasma samples with known quantities of human renin, evidence was obtained suggesting that factors other than enzyme or total substrate concentrations affect the velocity of angiotensin formation. This variability of reaction rate may be explained by the existence of an inhibitor or activator in this system or by a variation ...
1. Total exchangeable sodium was measured in rats by a radio-sodium equilibration method, before and after the production of hypertension by clipping the left renal artery, with or without contralateral nephrectomy.. 2. Clipping of one renal artery with removal of the other kidney produced severe hypertension with no significant changes in exchangeable sodium or plasma renin levels.. 3. Clipping of one renal artery without contralateral nephrectomy produced severe hypertension in some animals, but little change in blood pressure in others. The animals which developed severe hypertension had a marked increase in exchangeable sodium with a concomitant rise in plasma renin; the animals with smaller rises in blood pressure did not have these changes.. 4. The fact that both plasma renin levels and exchangeable sodium levels increase according to this method, suggests that hypertension in the two-kidney model is renin-dependent.. ...
A Genetic Variant in the Distal Enhancer Region of the Human Renin Gene Affects Renin Expression. . Biblioteca virtual para leer y descargar libros, documentos, trabajos y tesis universitarias en PDF. Material universiario, documentación y tareas realizadas por universitarios en nuestra biblioteca. Para descargar gratis y para leer online.
A comprehensive review of physiological and molecular biological evidence refutes claims for synthesis of renin by cardiac and vascular tissues. Cardiovascular tissue renin completely disappears after binephrectomy. Residual putative reninlike activity, where investigated, has had the characteristics of lysosomal acid proteases. Occasional reports of renin or renin mRNA in vascular and cardiac tissues can be ascribed to failure to remove the kidneys 24 hours beforehand, overloading of detection systems, problems with stringency in identification, and illegitimate transcripts after more than 25 cycles of polymerase chain reaction. Others, using more stringent criteria, have failed to detect cardiac and vascular renin mRNA. Accordingly, a growing number of investigators have concluded that the kidneys are the only source of cardiovascular tissue renin. Although prorenin is secreted from extrarenal tissues as well as from the kidneys, there is no evidence that it is ever converted to renin in the ...
Novel features of the present work include the extensive comparison of renin cells with numerous cells types from the renal cortex at different developmental points. Furthermore, we developed a single cell isolation and amplification procedure that allowed us to identify the transcriptome of individual adult JG cells. Specifically, we show that renin cells express a unique set of genes vastly different from other cell types in the kidney: They possess markers that topologically and functionally link them to arterial and interstitial pericytes, and express Akr1b7, a new and valuable marker for renin cells, independent from renin expression. Contrary to arteriolar cells distant from the glomerulus, which transiently express renin during development and/or a homeostatic threat, adult JG cells maintain a dual smooth muscle and renin phenotype, driven by a unique transcriptional network that maintains, at all cost, the cells dual endocrine and contractile functions necessary for the maintenance of ...
The results of the present study demonstrate the presence of increased concentrations of renin and prorenin in left ventricular tissue from patients with DCM. The cardiac levels of renin and prorenin were more than fivefold the cardiac levels in the donors. In addition, the cardiac tissue-to-plasma concentration ratios for renin and prorenin (molecular mass, 48 and 54 kD, respectively) were approximately threefold the ratio for serum albumin (molecular mass, 70 kD), indicating that the levels of renin and prorenin in cardiac tissue were too high to be explained by admixture with blood or by diffusion from the blood into the interstitial fluid. In normal porcine left ventricular tissue, the renin level was also higher than can be explained by its localization in extracellular fluid.4 Purified membrane fractions prepared from porcine left ventricular tissue contained renin,4 and specific binding of renin and prorenin to rat renal and other tissue membranes has been reported.35 36 In the present ...
1. In a prospective study involving fifty-six women, measurements of body weight, urinary creatinine, sodium and potassium and plasma sodium, potassium and renin activity were made in mid-pregnancy and at 36 weeks. The effect of sodium restriction and sodium loading on these measurements was assessed in mid-pregnancy.. 2. Mean plasma renin activity was significantly higher throughout pregnancy than the normal non-pregnant mean level. It was lower at 36 weeks than in mid-pregnancy in those whose pregnancy was normal but not in those who developed toxaemia of pregnancy between 38 and 40 weeks. In mid-pregnancy in both groups sodium depletion was significantly elevated but sodium loading did not significantly depress plasma renin activity.. 3. The urinary potassium/creatinine ratio in mid-pregnancy and urinary sodium/creatinine ratio at 36 weeks were lower in those who subsequently developed toxaemia, raising the possibility of a functional renal lesion which antedates the morphologically ...
The renin-angiotensin system (RAS) is a hormone system that regulates blood pressure and extracellular volume in the body. The RAS sequentially processes angiotensinogen to angiotensin II (Ang II), a peptide hormone that is a potent vasoconstrictor. Inhibition of RAS components has been used successfully in the treatment of hypertension, heart failure and end organ damage. Renin catalyzes the first and rate-limiting step of the RAS cascade and renin is specific for angiotensinogen. Blockade of Ang II production by direct inhibition of renin has long been a therapeutic goal. Early renin inhibitors, such as enalkiren and remikiren, were effective in blood pressure lowering. However, due to poor oral bioavailability, duration of action, and high costs of synthesis, these early peptidomimetic inhibitors never progressed to pivotal clinical studies [1]. Continued clinical interest in renin has led to the recent approval of the first renin inhibitor, aliskiren (Tekturna™), a non-peptidic inhibitor ...
BACKGROUND: The activity of the renin-angiotensin system is usually evaluated as plasma renin activity (PRA, ngAI/ml per h) but the reproducibility of this enzymatic assay is notoriously scarce. We compared the inter and intralaboratory reproducibilities of PRA with those of a new automated chemiluminescent assay, which allows the direct quantification of immunoreactive renin [chemiluminescent immunoreactive renin (CLIR), microU/ml]. METHODS: Aliquots from six pool plasmas of patients with very low to very high PRA levels were measured in 12 centres with both the enzymatic and the direct assays. The same methods were applied to three control plasma preparations with known renin content. RESULTS: In pool plasmas, mean PRA values ranged from 0.14 +/- 0.08 to 18.9 +/- 4.1 ngAI/ml per h, whereas those of CLIR ranged from 4.2 +/- 1.7 to 436 +/- 47 microU/ml. In control plasmas, mean values of PRA and of CLIR were always within the expected range. Overall, there was a significant correlation
Peptides , Angiotensins and Related Peptides , Peptide Substrate for Renin 520 Assay kit; This FRET peptide is a specific substrate for renin. Aspartyl protease cleaves angiotensinogen to yield angiotensin I, which is further converted to angiotensin II. The renin-angiotensin system is a coordinated hormonal cascade in the control of cardiovascular, renal, and adrenal function. It governs body fluid and electrolyte balance, as well as arterial pressure. Since an overactive renin-angiotensin system leads to hypertension, renin is an attractive target for the treatment of this disease. This renin peptide substrate may be used for screening of renin inhibitors. In the FRET peptide, the fluorescence of 5-FAM is quenched by QXL 520. Upon cleavage into two separate fragments by renin, the fluorescence of 5-FAM is recovered, and can be monitored at excitation/emission = 490/520 nm. This substrate is employed in the SensoLyte 520 Renin Assay Kit, cat # 72040.
1. A synthetic 3-([14C]valine)-labelled tetradecapeptide renin substrate was used to measure renin concentration. Renin liberated 14C-labelled angiotensin I, which was separated from the labelled substrate by paper chromatography. The conversion of substrate into angiotensin I was quantitated by liquid-scintillation counting of radioactivity. 2. The rate of conversion of the substrate into angiotensin I was shown to be linearly related to renin concentration and time under suitable conditions. Angiotensin generation measured in this system agrees well with that measured by bioassay. 3. It is suggested that the use of a pure substrate offers advantages that include the standardization of current units of renin measurement.. ...
TY - JOUR. T1 - Role of 18-hydroxylated cortisols in hypertension. AU - Gomez-Sanchez, Celso E.. AU - Gomez-Sanchez, elise P.. AU - Holland, O. Bryan. PY - 1987. Y1 - 1987. N2 - The isolation of 18-hydroxycortisol and 18-oxocortisol was recently described. These steroids have been shown to be excreted in exaggerated quantities in patients with primary aldosteronism, with adrenal adenomas and in glucocorticoid suppressible aldosteronism. We report the measurement of both steroids in the urine of patients with essential hypertension. 18-Oxocortisol excretion did not differ in patients with normal renin essential hypertension (0.7 ± 0.7 μg/24 h), low renine essential hypertension (0.7 ± 0.5 μg/24 h) and normal individuals (1.2 ±0.9 μg/24 h). Patients with normal renin hypertension excreted 54 ± 43 μg/24 h of 18-hydroxycortisol, those with low renin essential hypertension excreted 58 ± 54 μg/24 h, and normal individuals excreted 63 ± 36 βg/24 h. Three of the low renin and one of the ...
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Renin release into plasma has been used to investigate the drug dose-dependence of renin-angiotensin system inhibition because it is proportional to the interruption of the permanent negative feedback loop of angiotensin II on renin secretion. We inv
The renin-angiotensin-aldosterone system controls blood pressure and salt-volume homeostasis. Renin, which is the first enzymatic step of the cascade, is critically regulated at the transcriptional level. In the present study, we investigated the role of liver X receptor α (LXRα) and LXRβ in the regulation of renin. In vitro, both LXRs could bind to a noncanonical responsive element in the renin promoter and regulated renin transcription. While LXRα functioned as a cAMP-activated factor, LXRβ was inversely affected by cAMP. In vivo, LXRs colocalized in juxtaglomerular cells, in which LXRα was specifically enriched, and interacted with the renin promoter. In mouse models, renin-angiotensin activation was associated with increased binding of LXRα to the responsive element. Moreover, acute administration of LXR agonists was followed by upregulation of renin transcription. In LXRα-/- mice, the elevation of renin triggered by adrenergic stimulation was abolished. Untreated LXRβ-/- mice ...
The renin-angiotensin-aldosterone system controls blood pressure and salt-volume homeostasis. Renin, which is the first enzymatic step of the cascade, is critically regulated at the transcriptional level. In the present study, we investigated the role of liver X receptor α (LXRα) and LXRβ in the regulation of renin. In vitro, both LXRs could bind to a noncanonical responsive element in the renin promoter and regulated renin transcription. While LXRα functioned as a cAMP-activated factor, LXRβ was inversely affected by cAMP. In vivo, LXRs colocalized in juxtaglomerular cells, in which LXRα was specifically enriched, and interacted with the renin promoter. In mouse models, renin-angiotensin activation was associated with increased binding of LXRα to the responsive element. Moreover, acute administration of LXR agonists was followed by upregulation of renin transcription. In LXRα-/- mice, the elevation of renin triggered by adrenergic stimulation was abolished. Untreated LXRβ-/- mice ...
Hypertension is a chronic condition associated with an increased risk of mortality and morbidity. Renin is the enzyme responsible for converting angiotensinogen to angiotensin I, which is then converted to angiotensin II. Renin inhibitors are a new class of drugs that decrease blood pressure (BP) by preventing the formation of both angiotensin I and angiotensin II. To quantify the dose-related BP lowering efficacy of renin inhibitors compared to placebo in the treatment of primary hypertension.To determine the change in BP variability, pulse pressure, and heart rate and to evaluate adverse events (mortality, non-fatal serious adverse events, total adverse events, withdrawal due to adverse effects and specific adverse events such as dry cough, diarrhoea and angioedema). The Cochrane Hypertension Information Specialist searched the following databases for randomized controlled trials (RCTs) up to February 2017: the Cochrane Hypertension Specialized Register, the Cochrane Central Register of ...
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Utilizing cocultures of mouse renal juxtaglomerular cells with bovine microvascular endothelial cells, we have examined whether endothelial cells exert direct influence on renin secretion from renal juxtaglomerular cells. In the presence of endothelial cells both spontaneous and forskolin (10 microM) or isoproterenol (10 microM) stimulated renin release were markedly attenuated. The stimulatory effect of the calmodulin antagonist calmidazolium (10 microM) on renin secretion was not altered by endothelial cells, whereas the stimulatory effect of ethylisopropylamiloride (50 microM) an inhibitor of sodium-proton exchange was enhanced in the presence of endothelial cells. Indomethacin (10 microM) and NG-monomethyl-l-arginine (NMMA) (1 mM) used to inhibit cyclooxygenase activity and production of endothelium-derived relaxing factor (EDRF) decreased spontaneous renin release in the presence of endothelial cells only, but had no effect on forskolin stimulated renin secretion. Endothelin (1 microM) inhibited
Apart from their endocrine functions renin-expressing cells play an important functional role as mural cells of the developing preglomerular arteriolar vessel tree in the kidney. The recruitment of renin-expressing cells from the mesenchyme to the vessel wall is not well understood. Assuming that it may follow more general lines of pericyte recruitment to endothelial tubes we have now investigated the relevance of the platelet-derived growth factor (PDGF)-B-PDGFR-β signaling pathway in this context. We studied renin expression in kidneys lacking PDGFR-β in these cells and in kidneys with reduced endothelial PDGF-B expression. We found that expression of renin in the kidneys under normal and stimulated conditions was not different from wild-type kidneys. As expected, PDGFR-β immunoreactivity was found in mesangial, adventitial and tubulo-interstitial cells but not in renin-expressing cells. These findings suggest that the PDGF-B-PDGFR-β signaling pathway is not essential for the recruitment ...
The juxtaglomerular cells (JG cells, or granular cells) are cells in the kidney that synthesize, store, and secrete the enzyme renin. They are specialized smooth muscle cells mainly in the walls of the afferent arterioles, and some in the efferent arterioles, that deliver blood to the glomerulus. In synthesizing renin, they play a critical role in the renin-angiotensin system and thus in autoregulation of the kidney. Juxtaglomerular cells secrete renin in response to a drop in pressure detected by stretch receptors in the vascular walls, or when stimulated by macula densa cells. Macula densa cells are located in the distal convoluted tubule, and stimulate juxtaglomerular cells to release renin when they detect a drop in sodium concentration in tubular fluid. Together, juxtaglomerular cells, extraglomerular mesangial cells and macula densa cells comprise the juxtaglomerular apparatus. In appropriately stained tissue sections, juxtaglomerular cells are distinguished by their granulated cytoplasm. ...
TY - JOUR. T1 - Comparative effects of estrogen and antiestrogen on plasma renin substrate levels and hepatic estrogen receptors in the rat. AU - Kneifel, Mark A.. AU - Katzenellenbogen, Benita S.. N1 - Copyright: Copyright 2016 Elsevier B.V., All rights reserved.. PY - 1981/2. Y1 - 1981/2. N2 - Studies were undertaken to compare the effects of the estrogen ethinyl estradiol [llα-ethinylestradiol-17β (EE2)] and the antiestrogen U11.100A [l-(2-[p-(3, 4-dihydro-6-methoxy- 2 - phenyl -1 - naphthyl) phenoxy] ethyl) pyrrolidine hydrochloride (UA)] on rat liver. These compounds were assessed for their abilities to bind to estrogen-specific binding sites in liver cytosol, to translocate these sites to the nucleus, and to induce elevations of hepatic production of plasma renin substrate. Both compounds were shown to cause significant 2- to 4-fold increases in plasma renin substrate levels after sc injections at dosages of 25, 100, and 250 μg daily for 2 days to mature female rats, and two related ...
TY - JOUR. T1 - Renin processing in cultured juxtaglomerular cells of the hydronephrotic mouse kidney. AU - Berka, J. L.. AU - Alcorn, D.. AU - Ryan, G. B.. AU - Skinner, S. L.. AU - Weaver, D. A.. PY - 1993. Y1 - 1993. N2 - We examined renin processing in cultured juxtaglomerular (JG) cells of the hydronephrotic mouse kidney with immunocytochemical and biochemical techniques. Compared with JG cells in normal kidneys, there was less intense labeling for renin protein in mature granules of cultured JG cells. However, pro-renin labeling of transport vesicles and juvenile granules was maintained, suggesting incomplete passage of pro-renin through intermediate and mature granules. Immunogold evidence of exocytosis of mature granules containing renin protein was present at all stages. Labeling of transport vesicles for pro-renin, together with the absence of exocytosis of pro-renin from juvenile granules, indicated that pro-renin was exclusively released by a constitutive process. Active renin ...
The effects on blood pressure of an antiserum against pure human kidney renin were studied in conscious and anesthetized (pentobarbital, 24 mg X kg-1 i.p.) small new world monkeys (common marmosets). The antiserum inhibited the enzymatic activity of renin by 50% in a dilution of 1:45,000 in marmoset and 1:50,000 in human plasma. The antiserum (0.2 ml i.v.) decreased blood pressure in conscious marmosets on normal sodium intake by 15 +/- 5 (SD) mmHg and after salt depletion by 31 +/- 13 mmHg. A converting enzyme inhibitor (teprotide, 2 mg X kg-1 i.v.) induced a comparable fall in blood pressure: -16 +/- 10 and -30 +/- 10 mmHg, respectively. Similar effects were observed on blood pressure of anesthetized marmosets. The correlation between pretreatment plasma renin concentration and the maximum fall in blood pressure was significant and identical for the experiments with antiserum and teprotide. These results demonstrate that antisera against human renin can be used for the specific blockade of the ...
The renin-angiotensin-aldosterone system can be activated by sympathetic nervous input and is thought to have an important role in the prevalence of hypertension and cardiovascular risk in black Africans. We examined (1) the association between plasma renin responses to mental stress and a marker of sub-clinical atherosclerosis; and (2) associations between resting renin and 24-h ambulatory blood pressure. Participants were 143 urbanized black African men and women (43.1±7.7 years) drawn from a study of Sympathetic Activity and Ambulatory Blood Pressure in Africans (SABPA). After an overnight fast, participants completed the Stroop mental stress task. Blood samples were drawn during baseline and 10 min after the task to assess the concentration of active renin in plasma. Blood pressure assessments included continuous Finometer measures during the stress testing and 24-h ambulatory monitoring. Carotid intima-media thickness (CIMT) was measured using high-resolution ultrasound. Approximately 50% ...
A total of 42 cases of large symptomatic parapelvic or pararenal lymphatic cysts has been reported since 1890, of which 54% were associated with hypertension and 14% were bilateral. We report on a patient in whom during a 3-month period abdominal pain and distention developed successively on both sides associated with hypertension. Initially, ultrasound and computerized tomography revealed a large multicystic pararenal lymphatic mass on the right side and small parapelvic hilus lesions on the left side. Two months after resection and marsupialization of the large cyst on the right side the small hilus lesions on the left side developed into large pararenal cysts requiring the same therapeutic measures. Hypertension was reversible after surgery in both instances; at the second operation high preoperative and lower postoperative renin activity, active renin, total renin, aldosterone and atrial natriuretic factor in plasma were noted. Immunoreactive active and total renin levels in the ly
OBJECTIVE The term receptor-associated prorenin system (RAPS) refers to the pathogenic mechanisms whereby prorenin binding to its receptor dually activates the tissue renin-angiotensin system (RAS) and RAS-independent intracellular signaling via the receptor. The aim of the present study was to define the association of the RAPS with diabetes-induced retinal inflammation.. RESEARCH DESIGN AND METHODS Long-Evans rats, C57BL/6 mice, and angiotensin II type 1 receptor (AT1-R)-deficient mice with streptozotocin-induced diabetes were treated with (pro)renin receptor blocker (PRRB). Retinal mRNA expression of prorenin and the (pro)renin receptor was examined by quantitative RT-PCR. Leukocyte adhesion to the retinal vasculature was evaluated with a concanavalin A lectin perfusion-labeling technique. Retinal protein levels of vascular endothelial growth factor (VEGF) and intercellular adhesion molecule (ICAM)-1 were examined by ELISA. Retinal extracellular signal-regulated kinase (ERK) activation was ...
TY - JOUR. T1 - Modeling sex differences in the renin angiotensin system and the efficacy of antihypertensive therapies. AU - Leete, Jessica. AU - Gurley, Susan. AU - Layton, Anita T.. PY - 2018/4/6. Y1 - 2018/4/6. N2 - The renin angiotensin system is a major regulator of blood pressure and a target for many anti-hypertensive therapies; yet the efficacy of these treatments varies between the sexes. We use published data for systemic RAS hormones to build separate models for four groups of rats: male normotensive, male hypertensive, female normotensive, and female hypertensive rats. We found that plasma renin activity, angiotensinogen production rate, angiotensin converting enzyme activity, and neutral endopeptidase activity differ significantly among the four groups of rats. Model results indicate that angiotensin converting enzyme inhibitors and angiotensin receptor blockers induce similar percentage decreases in angiotensin I and II between groups, but substantially different absolute ...
I recently had my aldosterone and renin checked. The results were: Aldosterone 17.2, Renin 0.1, Aldosterone/Renin Ratio 172.0. For years Ive had low potassium and taking a potassium prescription whic...
Urinary kallikrein excretion (UKE) is decreased in rats with passive Heymann nephritis (PHN), but increases after converting enzyme inhibition (CEI). Although CEI potentiates bradykinin activity, neither the effect of CEI on kallikrein secretion nor the abnormal renal kallikrein metabolism in PHN has been examined previously. To determine the mechanism by which CEI increases UKE, normal rats and PHN received enalapril, 40 mg/kg per d orally for 4 d. UKE was 85% lower in PHN than in normals and increased in both groups after CEI, although UKE in PHN remained significantly less than in normals. Kallikrein mRNA was significantly lower in PHN compared to normals but not in PHN treated with CEI and did not change in normal rats. Renin mRNA was significantly lower in PHN, and was stimulated by CEI only in normals. Renal kallikrein and renin content were not different and were not altered by CEI. Both kallikrein and renin genes appear to be transcriptionally suppressed in rats with PHN and the ...
Pericytes, perivascular cells embedded in the microvascular wall, are crucial for vascular homeostasis. These cells also play diverse roles in tissue development and regeneration as multi-lineage progenitors, immunomodulatory cells and as sources of trophic factors. Here, we establish that pericytes are renin producing cells in the human kidney. Renin was localized by immunohistochemistry in CD146 and NG2 expressing pericytes, surrounding juxtaglomerular and afferent arterioles. Similar to pericytes from other organs, CD146(+)CD34(-)CD45(-)CD56(-) renal fetal pericytes, sorted by flow cytometry, exhibited tri-lineage mesodermal differentiation potential in vitro. Additionally, renin expression was triggered in cultured kidney pericytes by cyclic AMP as confirmed by immuno-electron microscopy, and secretion of enzymatically functional renin, capable of generating angiotensin I. Pericytes derived from second trimester human placenta also expressed renin in an inducible fashion although the renin activity
Aldosterone/renin ratio. ,2000 Conns likely if renin ,0.3 pmol/mL/h. 800 - 2000 Possibly Conns, investigate further. ,800 Conns unlikely. For diagnosis of Conns: low renin expected. Plasma renin ≤0.3 pmol/ml/hr (ref. 0.5-3.1). Aldosterone usually , 350 pmol/L (ref. 100-800) ie. may be normal or high. SECOND LINE INVESTIGATION: CONFIRMATION OF PRIMARY HYPERALDOSTERONISM Saline infusion test:. Stop spironolactone and epelerone for 6 weeks before the test. Stop beta blockers, calcium channel antagonists, ACE inhibitors and AT2 blockers for 2 weeks before the test.. Can continue to use alpha blockers to manage hypertension eg doxazosin. Ensure plasma K in normal range (ideally ,4) prior to performing test. Examine patient for signs of cardiac failure. This test should not be performed in patients with severe uncontrolled hypertension, renal insufficiency, cardiac insufficiency, cardiac arrhythmia, or severe hypokalemia.. Patients stay in the recumbent position for at least 1 hour before test ...
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Install Plasma Active on ARM Systems = == External MultiMediaCard (MMC) Images == === Mer Plasma Active === The [http://merproject.com Mer] project creates a Plasma Active [http://bug10738.openaos.org/images/tegra2/ MMC Image] which is build for the armv7hl target devices like the ARM Tegra 2 tablet. For more details please see the related [http://wiki.merproject.com/wiki/Community_Workspace Mer Wiki]. You can also download the kernel boot image, the external MMC image and some additional helper scripts from basysKom download location [http://share.basyskom.com/contour/Deployment/latest-basyskom-plasma-active-tegra2-mer.html here]. == Deploying a Plasma Active (MMC) raw Image to a MultiMediaCard == A Installation description for MultiMediaCards could be found in the [http://wiki.meego.com/ARM/N900/Install/MMC MeeGo ARM Wiki]. = Install Plasma Active on x86 Systems = == Live Images== These can be used as testing base and to track progress. === Balsam Professional === [http://open-slx.de open-slx] ...
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Rabbit anti human prorenin IgG fraction, high titer - Polyclonal antibody (host rabbit) to human renin. Affinity purified by immobilized human prorenin.
Inhibitory monoclonal antibody to human prorenin, clone 4B5-E3 - This antibody only binds prorenin. It does not bind renin and blocks prorenin activation.
Mast cells are connected with swelling and fibrosis. led to renin-dependent protracted circulation recovery. This demonstrates that mast cell renin is PIK-294 supplier definitely energetic in situ and the following ANG II can modulate intrarenal vascular level of resistance in the UUO kidney. Jointly, the data Rabbit Polyclonal to STEA3 demonstrate that mast cells are essential to the advancement of renal fibrosis in the 14-day time UUO kidney. Since renin is definitely present in human being kidney mast cells, our function recognizes potential focuses on in the treatment of renal fibrosis. is definitely the quantity of photo slides for a provided pet. Renin activity (ANG I radioimmunoassay). Renin activity was assessed in separated mast cell lysate (rat kidney and human being kidney), as previously reported (32, 48, 54). The recognition limit was 0.01 pmol (32). Remote mast cells had been lysed in 1 ml of PBS by four cycles of freeze-thaw. The renin-containing lysates had been after that ...
http://youtu.be/iAZmLkSCmY0 GIMA AMEZIA SARI G1F011016 DESKRIPSI Renin adalah enzim dengan protein kecil yang dilepaskan oleh ginjal bila tekanan arteri turun sangat rendah. Pengeluaran renin dapat disebabkan aktivasi saraf simpatis (pengaktifannya melalui β1-adrenoceptor) (Guyton dan Hall,1997). Angiotensin adalah hormone petida yang berasal dari protein angiotensinogen. Angiotensinogen di ubah menjadi angiotensin 1 dengan katalisis renin. Selanjutnya angiotensin…
TY - JOUR. T1 - Aging and aldosterone. AU - Hegstad, Rebecca. AU - Brown, Ronald D.. AU - Jiang, Nai Siang. AU - Kao, Pai. AU - Weinshilboum, Richard M.. AU - Strong, Cameron. AU - Wisgerhof, Max. PY - 1983/3. Y1 - 1983/3. N2 - We measured urinary and plasma aldosterone in normal subjects, aged 20 to 59 years, during a period of unrestricted sodium intake and after sodium depletion, using furosemide or a 20 meq sodium diet. Before and after sodium depletion, the mean and the upper limit of the range of urinary aldosterone excretion were considerably lower in subjects over 50 years compared with subjects under 30 years. Aging had no effect on plasma aldosterone concentration when the subjects were on an unrestricted sodium diet and blood was sampled while they were recumbent. In contrast, when the subjects were upright, both before and after sodium depletion, the mean and the upper limit of the range of plasma aldosterone concentration were lower in the subjects over 50 years compared with those ...
Antiserum specific for purified canine renal renin was used to inhibit this enzyme in trained, conscious dogs. The antiserum did not affect blood pressure in sodium-replete dogs but decreased plasma renin activity and blood pressure in sodium-depleted animals. The antiserum also reduced blood pressure to control levels concomitant with suppression of plasma renin activity in uninephrectomized dogs with acute renovascular hypertension. These observations establish the role of the renin-angiotensin system in the maintenance of blood pressure in the sodium-depleted state as well as in the initiation of renovascular hypertension. ...
TY - JOUR. T1 - Increased Vascular Sensitivity to Angiotensin II in Psychosocial Hypertensive Mice. AU - Clinton Webb, R.. AU - Johnson, Joyce C.. AU - Vander, Arthur J.. AU - Henry, James P.. PY - 1983/1/1. Y1 - 1983/1/1. N2 - CBA mice develop hypertension when placed in complex population cages that facilitate social interactions and competition for territory. After 1 month, these mice have normal plasma renin levels, but blockade of converting enzyme lowers blood pressure to normal. To test the possibility that this normal-renin hypertension is caused by enhanced pressor responsiveness to angiotensin II (All), we examined the effects of All on hindquarter and renal vasculatures from 13 hypertensive and 13 normotensive mice. Both vascular beds were pump-perfused at a constant flow with plasma substitute. Optimal perfusion flows and basal pressures were similar in hindquarter (8 ml/100 g/min; 60 mm Hg) and renal vasculatures (130 ml/100 g/min; 50 mm Hg) from normotensive and hypertensive mice. ...
The discrepant and partially independent effects of the various RAS peptides and enzymes on immune responses should allow discrete, optimized interventions to limit RAS-dependent inflammation in humans. AT2 receptor and Ang 1-7 agonists, if carefully engineered and tested in specific cardiovascular and renal disease contexts, may complement current ACEI and ARB treatment, possibly by mitigating the induction of inflammatory responses that can result from blocking AT1 receptors on immune cells. Inasmuch as noncanonic renin/prorenin signaling provokes inflammatory responses independently of Ang II, direct renin inhibition may similarly complement standard RAS blockade by suppressing immunity. In this regard, human studies confirm the favorable effects of direct renin inhibition on parameters of immune activation. For example, in 27 patients with type 1 diabetes mellitus and no nephropathy, treatment with aliskerin for 30 days reduced urinary excretion of IFN-α2 and IL-2.77 Similarly, in 30 ...
Renin Activity Fluorometric Assay Kit: simple, rapid & convenient method to detect renin activity as low as 0.75 U/ml. 100 assays.
PubMed journal article: Developmental renin expression in mice with a defective renin-angiotensin system. Download Prime PubMed App to iPhone, iPad, or Android
Renin aktivira renin-angiotenzin cijepanjem angiotensinogena, u produkciji jetre, pa nastaje angiotenzin I, koji se dalje pretvara u angiotenzina II pomoću angiotenzin-konvertirajućeg enzima (ACE), angiotenzin konvertirajućeg enzima, prije svega u kapilarima pluća. Angiotenzina II zatim sužava krvne sudove, povećava lučenje antidiuretskog hormona (ADH) i aldosteronaa, a stimulira hipotalamus da aktivira refleks žeđi, što doveli do povećanja krvnog pritiska. Primarna funkcija renina je stoga da na kraju izaziva povećanje krvnog pritiska, što dovodi do obnove perfuzije pritiska u bubrezima. Renin se luči iz jukstaglomerulskih bubrežnih ćelija, što izaziva promjene u bubrežnom perfuzijskom pritisku, preko dionice receptora u zidova krvnih sudova. Jukstaglomerulske ćelije su također, putem ćelijske signalizacije, stimulirane da oslobode renin. Macula densa čulo mijenja volumen distalnih tubula i odgovara na pad tubulskog volumena, stimulacijom oslobađanja renina u ...
TY - JOUR. T1 - Expression of cytochrome P45011B1 mRNA in the brain of normal and hypertensive transgenic rats. AU - Erdmann, Bettina. AU - Gerst, Hellmut. AU - Lippoldt, Andrea. AU - Buelow, Hannes E.. AU - Ganten, Detlev. AU - Fuxe, Kjell. AU - Bernhardt, Rita. PY - 1996/9/9. Y1 - 1996/9/9. N2 - Cytochrome P45011B1 (11β-hydroxylase) was detected in the brain of male rats by in situ hybridization methods. Normal Sprague-Dawley rats were compared to the transgenic strain TGR(mRen2)27, characterized by the expression of the murine Ren-2(d) renin gene and the development of severe hypertension. Specific riboprobes were generated by in vitro transcription of a 152 base-pair long cDNA template. 35S-labeled riboprobes were hybridized to cryostat sections from adrenal glands and from two different levels of the brain using standard protocols and varying washing conditions. After exposure of the radiolabeled sections to X-ray film, the signals were quantified and compared. Following autoradiography ...
TY - JOUR. T1 - Thiazide (TZ) induced increase in salt and water appetite is mediated by the renin angiotensin system, not by volume or osmolality. AU - OConnor, D. T.. AU - Preston, R. A.. AU - Stone, R. A.. PY - 1978/1/1. Y1 - 1978/1/1. UR - http://www.scopus.com/inward/record.url?scp=0018115740&partnerID=8YFLogxK. UR - http://www.scopus.com/inward/citedby.url?scp=0018115740&partnerID=8YFLogxK. M3 - Article. AN - SCOPUS:0018115740. VL - 14. JO - Kidney International. JF - Kidney International. SN - 0085-2538. IS - 6. ER - ...
The renin-angiotensin system (RAS) or the renin-angiotensin-aldosterone system (RAAS) is a hormone system that regulates blood ... Fetal renin-angiotensin system[edit]. In the fetus, the renin-angiotensin system is predominantly a sodium-losing system,[ ... Direct renin inhibitors can also be used for hypertension.[16] The drugs that inhibit renin are aliskiren[17] and the ... Local renin-angiotensin systems[edit]. Locally expressed renin-angiotensin systems have been found in a number of tissues, ...
Renin-e Bozorg , Renin-e Kuchek , Reza Alichi , Rezayi , Rezvan , Rig Deraz , Rig Kag , Rig Muled , Rig , Rig , Rigu , Riku , ...
... low renin and low ACTH indicates atrophy of aldosterone production from the prolonged lack of renin. Similar to the cortisol ... "Aldosterone and Renin". Archived from the original on 2008-09-17. Retrieved 2008-08-18. Cite journal requires ,journal= (help) ... This factoring indicates secondary hypoaldosteronism (sodium low, potassium and renin enzyme will be low). Usually doubling to ... potassium and renin enzyme will be high) and is an indicator of primary adrenal insufficiency or Addison's disease.[citation ...
... is an antagonist to renin. Renin, the first enzyme in the renin-angiotensin-aldosterone system, plays a role in blood ... Aliskiren (brand names Tekturna and Rasilez) is the first in a class of drugs called direct renin inhibitors. It is used for ... Therefore, pharmacologists have been looking for a drug to inhibit renin directly. Aliskiren is the first drug to do so. "First ... PharmaXChange: Direct Renin Inhibitors as Antihypertensive Drugs Archived 2010-12-07 at the Wayback Machine "Aliskiren". Drug ...
Blood pressure and fluid and electrolyte homeostasis is regulated by the renin-angiotensin-aldosterone system.Renin, an enzyme ... 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- ... In 1939, renin was found not to cause the rise in blood pressure, but was an enzyme which catalyzed the formation of the ... Their results suggested the kidneys produced a protein, which they named renin, that caused a rise in blood pressure. In the ...
His research career centered on the [Renin Angiotensin System , renin-angiotensin system]. While at the Universities of Tuzla ... The renin-angiotensin system and its blockers. Igić R, Škrbić R. Srp Arh Celok Lek. 2014 Nov-Dec;142(11-12):756-63. doi: ... Activity of renin and angiotensin converting enzyme in retina and ciliary body. (In Serbo-croatian). Liječ Vjes 1977;99:482-4. ... Igić R, Škrbić R. The renin-angiotensin system and its blockers. Srp Arh Celok Lek 2014;142:756-63. Sokolova-Djokic L, Zizic- ...
Renin and Angiotensin". In Brunton LL, Chabner B, Knollmann BC (eds.). Goodman & Gilman's The Pharmacological Basis of ... The packaging for valsartan includes a warning stating the drug should not be used with the renin inhibitor aliskiren in people ... The U.S. prescribing information lists the following drug interactions for valsartan: Other inhibitors of the renin-angiotensin ... October 2014). "Co-trimoxazole and sudden death in patients receiving inhibitors of renin-angiotensin system: population based ...
Over time, these increases in workload, which are mediated by long-term activation of neurohormonal systems such as the renin- ... Vasopressin levels are usually increased, along with renin, angiotensin II, and catecholamines to compensate for reduced ... renin-angiotensin system inhibitors; and beta-blockers. In 2011, nonhypertensive heart failure was one of the 10 most expensive ...
The elevated blood pressure seen in Page kidney is thought to be caused by the activation of the renin-angiotensin-aldosterone ... This decrease in blood flow is recognized by the juxtaglomerular (JG) cells and promotes the cleavage of prorenin into renin. ... The compression is believed to cause activation of the renin-angiotensin-aldosterone system (RAAS) via microvascular ischemia. ... Fountain, JH; Lappin, SL (July 27, 2020). Physiology, Renin Angiotensin System. Treasure Island, FL: StatPearls Publishing. ...
"Renin-positive granulated Goormaghtigh cells. Immunohistochemical and electron-microscopic studies on biopsies from patients ... although it has been associated with the secretion of erythropoietin and secretion of renin. They are distinguished from ... and play a role in renal autoregulation of blood flow to the kidney and regulation of systemic blood pressure through the renin ...
Paul, Renin (7 March 2006). "GM reduces Suzuki alliance by 17.4 percent to raise $2bn". Earthtimes.com. Webster, Mark (2002), ...
Direct renin inhibitors - e.g. Co-Rasilez or Tekturna HCT (with aliskiren) Potassium sparing diuretics: Dyazide and Maxzide ...
Succinate serves as a modulator of blood pressure by stimulating renin release in macula densa and juxtaglomerular apparatus ... Peti-Peterdi, János; Gevorgyan, Haykanush; Lam, Lisa; Riquier-Brison, Anne (2012-06-23). "Metabolic control of renin secretion ...
"Renin-angiotensin system blockade: Finerenone". Nephrologie & Therapeutique. 13 Suppl 1: S47-S53. doi:10.1016/j.nephro.2017.02. ...
Sumners C, Horiuchi M, Widdop RE, McCarthy C, Unger T, Steckelings UM (2013). "Protective arms of the renin-angiotensin-system ... Angiotensin II is an octapeptide hormone central to the renin-angiotensin system. It regulates blood pressure control, water ... Receptor agonists and antagonist of angiotensin II receptors that target various parts of the complicated renin-angiotensin ... Alterman M. (2010). "Development of selective non-peptide angiotensin II type 2 receptor agonists". J Renin Angiotensin ...
Renin-angiotensin system: The kidneys sense low blood pressure. Release renin into the blood. Renin causes production of ...
... discovered renin at the Karolinska Institute, Stockholm in 1898. Renin is a component of the renin-angiotensin system which ... Tigerstedt's work on renin was probably inspired by Brown-Sequard's work examining the effect of organ extracts on ... They further showed that the pressor effect of renin did not require an intact nervous system and that it was not accompanied ... They concluded that renin caused vasoconstriction, but the mechanism was unknown. This question would remain unresolved until ...
... erythropoietin and renin); the thymus; skin (cholecalciferol); and adipose tissue (leptin and resistin). Endocrine glands ...
In the opposite case, juxtaglomerular cells are stimulated to release more renin, which stimulates the renin-angiotensin system ... Homeostasis Renin-angiotensin system "CV Physiology , Autoregulation of Organ Blood Flow". www.cvphysiology.com. Retrieved 2020 ... and juxtaglomerular cells in both the afferent and efferent arteriole decrease their renin secretion. These actions function to ...
Oelkers W (February 2002). "The renin-aldosterone system and drospirenone". Gynecol. Endocrinol. 16 (1): 83-7. doi:10.1080/gye. ... thereby activating the renin-angiotensin-aldosterone system. As a result, they can produce undesirable side effects including ... and produces compensatory increases in plasma renin activity as well as circulating levels and urinary excretion of aldosterone ...
This activates the renin-angiotensin system. Among other actions, it causes renal tubules (i.e. the distal convoluted tubules ... The activated renin-angiotensin system stimulates the zona glomerulosa of the adrenal cortex which in turn secretes the hormone ...
Garovic, Vesna D. (2006). "Monogenic Forms of Low-Renin Hypertension". Nature Clinical Practice. Nephrology. Nature Clinical ... hypertension and lowered renin levels. The hyperkalemia found in PHA2 is proposed to be a function of diminished sodium ...
Oakes, Joshua M.; Fuchs, Robert M.; Gardner, Jason D.; Lazartigues, Eric; Yue, Xinping (2018). "Nicotine and the renin- ...
Renin elevation is another risk factor. Renin is an enzyme secreted by the juxtaglomerular apparatus of the kidney and linked ... Vitamin D inhibits renin secretion and its activity, it therefore acts as a "negative endocrine regulator of the renin- ... High renin levels predispose to hypertension by causing sodium retention through the following mechanism: Increased renin → ... Low-renin hypertension is more common in African Americans than white Americans, and may explain why African Americans tend to ...
Excess secretion of renin by the juxtaglomerular cells can lead to excess activity of the renin-angiotensin system, ... Renin is produced by juxtaglomerular cells. These cells are similar to epithelium and are located in the tunica media of the ... Renin is also found in these cells. At the point where the afferent arterioles enter the glomerulus and the efferent arteriole ... One cause of this can be increased renin production due to narrowing of the renal artery, or a tumour of juxtaglomerular cells ...
DeMello WC, Re RN (2009). "Systemic versus local renin angiotensin systems. An overview.". In DeMello WC, Frohlich ED (eds.). ... Fimasartan acts on the kidney's rennin-angiotensin cascade, which begins when renin release from the kidney causes the ... Renin angiotensin system and cardiovascular disease. New York, NY: Humana Press. pp. 1-5. ISBN 978-1-60761-186-8. "Fimasartan ...
Renin but not aldosterone is elevated. Many infants born with this condition died before a method for diagnosis was recognized ...
Renin comes one level higher than angiotensin converting enzyme (ACE) in the renin-angiotensin system. Renin inhibitors can ... Aliskiren (developed by Novartis) is a renin inhibitor which has been approved by the U.S. FDA for the treatment of ... Levy BI (September 2005). "How to explain the differences between renin angiotensin system modulators". American Journal of ... Mehta, Akul (January 1, 2011). "Direct Renin Inhibitors as Antihypertensive Drugs". Archived from the original on 21 February ...
... and REN encoding renin (chromosome 1q32.1). Eckardt, KU; Alper, SL; Antignac, C; Bleyer, AJ; Chauveau, D; Dahan, K; Deltas, C; ... A third form of the disease occurs due to mutations in the gene encoding renin (ADTKD-REN), and has formerly been known as ...
"Renin gene haplotype diversity and linkage disequilibrium in two Mexican and one German population samples". Journal of the ... Renin-Angiotensin-Aldosterone System. 12 (3): 231-237. doi:10.1177/1470320310388440. PMID 21163863. S2CID 26481247. Martinez- ...
The renin-angiotensin system (RAS) or the renin-angiotensin-aldosterone system (RAAS) is a hormone system that regulates blood ... Fetal renin-angiotensin system[edit]. In the fetus, the renin-angiotensin system is predominantly a sodium-losing system,[ ... Direct renin inhibitors can also be used for hypertension.[16] The drugs that inhibit renin are aliskiren[17] and the ... Local renin-angiotensin systems[edit]. Locally expressed renin-angiotensin systems have been found in a number of tissues, ...
Renin can also be referred to as a hormone, as it has a receptor, the (pro)renin receptor, also known as the renin receptor and ... The normal concentration of renin in adult human plasma is 1.98-24.6 ng/L in the upright position. Renin activates the renin- ... Angiotensin-converting enzyme Plasma renin activity Renin inhibitor Renin stability regulatory element (REN-SRE) GRCh38: ... all of which may produce renin. Renin is usually measured as the plasma renin activity (PRA). PRA is measured specially in case ...
Plasma Renin Activity Congenital Adrenal Hyperplasia Primary Aldosteronism Plasma Aldosterone Zona Glomer These keywords were ... Homer, J. M., Hintz, R. L., and Luetscher, J. A., 1979, The role of renin and angiotensin in salt-losing, 21-hydroxylase ... Lemal, J. M., Rapaport, R., and Bayard, F., 1976, Plasma aldosterone, renin activity, and 17a-hydroxyprogesterone in salt- ... Biglieri E.G. (1985) Aldosterone and Renin. In: Ingbar S.H. (eds) Contemporary Endocrinology. Contemporary Endocrinology (( ...
"Purification and properties of renin and gamma-renin from the mouse submaxillary gland". The Journal of Biological Chemistry. ... Gamma-renin (EC 3.4.21.54) is an enzyme. This enzyme catalyses the following chemical reaction Cleavage of the Leu-Leu bond in ... Gamma-renin at the US National Library of Medicine Medical Subject Headings (MeSH) Biology portal. ... Drinkwater CC, Evans BA, Richards RI (June 1988). "Sequence and expression of mouse gamma-renin". The Journal of Biological ...
Renin is a hormone that controls the production of aldosterone, a hormone made in the adrenal glands. The two hormones are ... A renin test measures renin levels in the blood. ... What is a renin test?. This test measures the level of renin in ... Other names: renin blood test, plasma renin activity (PRA) aldosterone-renin ratio (ARR) ... A renin test (or renin and aldosterone test) is used to find out if the adrenal glands are making too much or too little ...
InterPro provides functional analysis of proteins by classifying them into families and predicting domains and important sites. We combine protein signatures from a number of member databases into a single searchable resource, capitalising on their individual strengths to produce a powerful integrated database and diagnostic tool.
Renin in Experimental Hypertension. Br Med J 1942; 2 doi: https://doi.org/10.1136/bmj.2.4258.179 (Published 15 August 1942) ...
Low plasma renin activity due to volume expansion is a feature common to these disorders; the disorders can be characterized ... Table 1. Characteristics of and Treatments for Monogenic Forms of Low-renin Hypertension. Disorder. Age of onset. Pattern of ... Table 1. Characteristics of and Treatments for Monogenic Forms of Low-renin Hypertension. Disorder. Age of onset. Pattern of ...
Molecules that are dissolved in water may dissociate into charged ions. An acid is a substance that increases the number of H+ ions in a solution. A base is a substance that decreases the number of H+ ions in a solution. The concentration of H+ ions in a solution can be measured and is called the pH of the solution.. The pH of a solution can be measured using a scale that ranges from 0 to 14. A solution of pH = 7 is neutral, a solution of pH lower than 7 is acidic, and a solution of pH greater than 7 is basic (alkaline). The number of H+ ions increases as the pH number decreases (and vice versa). The difference between two successive numbers on the pH scale represents a ten-fold difference in the H+ ion concentration because the scale is a logarithmic scale (log of base 10). For example, a solution with a pH of 2 has 10 times more H+ ions as a solution with a pH of 3. A solution with a pH of 2 has 100 times more H+ ions as a solution with a pH of 4. ...
Random plasma renin; PRA. Learn more about this test here. ... the level of renin in blood.Alternative Names Plasma renin ... Most often, the renin blood test is done at the same time as an aldosterone blood test to calculate the renin to aldosterone ... Be aware that renin level can be affected by pregnancy, as well as the time of day and the body position when blood is drawn. ... Renin is a protein (. enzyme. ) released by special kidney cells when you have a decreased salt (sodium) level or low blood ...
It has been theorized that dual blockade of the renin-angiotensin-aldosterone system (RAAS) might prove even more beneficial, ... It has been theorized that dual blockade of the renin-angiotensin-aldosterone system (RAAS) might prove even more beneficial, ... Combination therapy also proved unsafe in the ALTITUDE trial, which tested the direct renin inhibitor aliskiren in addition to ...
In this way, they discovered renin. This paper covers the methods by which its mode of action was uncovered, as well as its ...
Renin, Genes, and Beyond. 40 Years of Molecular Discoveries in the Hypertension Field. Brian J. Morris ...
Helping you find trustworthy answers on Renin-Angiotensin System , Latest evidence made easy ... Find all the evidence you need on Renin-Angiotensin System via the Trip Database. ... Blockade of the Renin-angiotensin-aldosterone System in Patients With ARVD Blockade of the Renin-angiotensin-aldosterone System ... Interactions Among Vitamin D, Atrial Fibrillation, and the Renin-Angiotensin-Aldosterone System. Blockade of the renin- ...
Helping you find trustworthy answers on Renin-Angiotensin System , Latest evidence made easy ... Find all the evidence you need on Renin-Angiotensin System via the Trip Database. ... Renin angiotensin system in liver diseases: Friend or foe? Full Text available with Trip Pro. Renin angiotensin system in liver ... Renin angiotensin system deregulation as renal cancer risk factor Full Text available with Trip Pro. Renin angiotensin system ...
Plasma renin activity definition at Dictionary.com, a free online dictionary with pronunciation, synonyms and translation. Look ... The estimation of renin in plasma by measuring the rate of formation of angiotensin I or II. ...
Currently there is great interest not only in the control of renin in the kidney, the sole source of circulating renin, but ... Cultured human uterine-placental cells expressed the human renin gene at levels higher than in other cell types assessed. Renin ... Thus, cAMP may activate renin gene expression under certain circumstances and tissue-specific renin gene expression may be ... Molecular biology of human renin and its gene.. Baxter JD1, Duncan K, Chu W, James MN, Russell RB, Haidar MA, DeNoto FM, Hsueh ...
Plasma renin levels were also measured in 116 treated hypertensive patients. There was no relation between plasma renin level ... Plasma Renin Levels and Vascular Complications in Hypertension Br Med J 1973; 2 :206 ... Plasma renin levels, measured in 39 untreated patients in 1967, under conditions of sodium loading and sodium depletion have ... Renin levels were not significantly different in patients with or without vascular complications. Out of 13 patients with ...
Second Edition updates new findings on the local renin-angiotensin systems (RAS) with a focus on the local RAASs of the ... The Local Cardiac Renin-Angiotensin Aldosterone System, Second Edition updates new findings on the local renin-angiotensin ... Renin Cell Identity and Homeostasis R. Ariel Gómez, Maria Luisa S. Sequeira Lopez, Xuan Jin, Magali Cordaillat, Ellen Steward ... Renin-Angiotensin-Aldosterone System and Cardiomyocyte Apoptosis in Hypertensive Heart Disease Arantxa González, Susana Ravassa ...
"Renin-dependent cardiovascular functions and renin-independent blood-brain barrier functions revealed by renin-deficient mice ... 2. Systemic and Brain Renin Angiotensin System. The renin angiotensin system (RAS) is a peptide hormone cascade that controls ... S. Inaba, M. Iwai, M. Furuno et al., "Continuous activation of renin-angiotensin system impairs cognitive function in renin/ ... Figure 4: A schematic representation of the renin-angiotensin system. Additional components of the renin-angiotensin system ( ...
The renin super-enhancers play a key role in the molecular memory of renin cell function, a mechanism at the core of preserving ... This induction of renin relies in part on the "memory" of cells in the kidney that produced renin during development and can ... Renin is highly conserved across multiple species from humans to Zebrafish (1). In humans, the renin gene rests on chromosome 1 ... During embryonic development, renin cells are progenitors for multiple cell types that retain the memory of the renin phenotype ...
Our efforts led to the discovery of compound (+)-26g that inhibits renin with an IC(50) of 0.20 nM in buffer and 19 nM in ... Design and preparation of potent, nonpeptidic, bioavailable renin inhibitors.. Bezençon O1, Bur D, Weller T, Richard-Bildstein ... The substituents attached at the positions 6 and 7 were essential for the binding affinity of these compounds for renin. The ... Starting from known piperidine renin inhibitors, a new series of 3,9-diazabicyclo[3.3.1]nonene derivatives was rationally ...
The library was screened for human renin sequences by hybridization with the previously cloned mouse renin cDNA. Of the 240,000 ... Cloning and sequence analysis of cDNA for human renin precursor. T Imai, H Miyazaki, S Hirose, H Hori, T Hayashi, R Kageyama, H ... Cloning and sequence analysis of cDNA for human renin precursor. T Imai, H Miyazaki, S Hirose, H Hori, T Hayashi, R Kageyama, H ... Cloning and sequence analysis of cDNA for human renin precursor. T Imai, H Miyazaki, S Hirose, H Hori, T Hayashi, R Kageyama, H ...
5. Renin-Angiotensin-System-Induced Sympathetic Overactivation in MetS. Both SNS and RAS are activated in obesity, and both ... A. D. de Kloet, E. G. Krause, and S. C. Woods, "The renin angiotensin system and the metabolic syndrome," Physiology and ... 4. Renin-Angiotensin System Activation in MetS. Previous many studies have demonstrated that RAS is activated in various organs ... Sympathoexcitation Associated with Renin-Angiotensin System in Metabolic Syndrome. Takuya Kishi1 and Yoshitaka Hirooka2 ...
Renin-angiotenzin sistem. Reference[uredi - уреди , uredi izvor]. *↑ Donald Voet, Judith G. Voet (2005). Biochemistry (3 izd ... Renin (lat. ren = bubreg) je enzim, koji se produkuje u bubrezima.[1][2][3] Izlučuje se u bubrezima prilikom pada krvnog ... regulacije krvne zapremine putem renin-angiotensina. • regulacija MAPKKK kaskade. • ćelijska maturacija. • proteoliza. • ... Kao proteaza, renin preobražava neaktivni angiotenzinogen u angiotenzin I. Ovaj zadnji se opet u jetri pod uticajem ACE-a ( ...
Our mission is to build healthier lives, free of cardiovascular diseases and stroke. That single purpose drives all we do. The need for our work is beyond question. Find Out More about the American Heart Association. ...
... and what the results of aldosterone and renin tests might mean ... Describes when aldosterone and renin tests are requested, how ... Normally when renin increases, aldosterone increases; when renin is low, aldosterone decreases. ... the most important of these being renin and angiotensin II. Renin, produced by the kidney, stimulates production of angiotensin ... Renin is then measured in these blood samples. If the value is significantly higher in one side, this indicates the site of the ...
... or the renin-angiotensin-aldosterone system (RAAS) is a hormone system that helps regulate ... Renin-angiotensin system The renin-angiotensin system (RAS) ... The renin-angiotensin system (RAS) or the renin-angiotensin- ... Fetal renin-angiotensin system In the fetus, the renin-angiotensin system is predominantly a sodium-losing system, as ... Renin cleaves an inactive peptide called angiotensinogen, converting it into angiotensin I. ...
... renin-angiotensin system; RAAS, renin-angiotensin-aldosterone system; t-PA, tissue plasminogen activator; and VIF, ... Expanding Saga of the Renin-Angiotensin System. The Angiotensin II Counter-Regulatory AT2 Receptor Pathway. Bodh I. Jugdutt ... renin-angiotensin system. The search for hidden truths behind established concepts and dogma is often a never-ending, uphill ... Targeting the renin-angiotensin system for the reduction of cardiovascular outcomes in hypertension: angiotensin-converting ...
Renin is synthesized as an enzymatically inactive proenzyme which is constitutively secreted from several tissues. Only renin- ... The aspartyl protease renin is the rate limiting activity of the renin-angiotensin-aldosterone system (RAAS). ... The aspartyl protease renin is the rate limiting activity of the renin-angiotensin-aldosterone system (RAAS). Renin is ... Only renin-expressing cells in the kidney are capable of generating active renin from prorenin, which is stored in prominent ...
  • Intrarenal renin - angiotensin system activation in end-stage renal disease 28179627 2018 07 30 2018 12 02 1348-4214 40 4 2017 04 Hypertension research : official journal of the Japanese Society of Hypertension Hypertens. (tripdatabase.com)
  • Are Local Renin-Angiotensin Systems the Focal Points for Understanding Salt Sensitivity in Hypertension? (springer.com)
  • Renin-angiotensin system (RAS) is activated in metabolic syndrome (MetS), and RAS inhibitors are preferred for the treatments of hypertension with MetS. (hindawi.com)
  • In the pathogenesis of MetS, renin-angiotensin system (RAS) is activated in various organs and tissues [ 3 - 6 ], and RAS inhibitors, such as angiotensin converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs), are preferred for the treatments of hypertension with MetS because of the prominent depressor effect with the improvement of insulin resistance [ 7 - 9 ]. (hindawi.com)
  • The story of the renin-angiotensin system (RAS), hypertension, and kidney disease began nearly 2 centuries ago, 1 with report of a clinico-pathophysiologic study of albuminuria in patients followed by Goldblatt's induction of hypertension in experimental dogs in the 1930s. (ahajournals.org)
  • This review aims to briefly address the state of knowledge of these various aspects of renin synthesis and secretion and attempts to relate them to the in vivo situation, in particular in men.American Journal of Hypertension (2012). (biomedsearch.com)
  • The authors report that, because of reactive renin secretion, this drug has not been any more effective than those already widely available to control hypertension. (webwire.com)
  • states, Aliskiren s pervasive stimulation of varying degrees of renin secretion could especially be a problem for those hypertensive patients who have hyper reactive renin systems such as patients with renovascular, advanced or malignant hypertension, all of whom were excluded from the trials. (webwire.com)
  • The article is Aliskiren, The First Renin Inhibitor for Treating Hypertension: Reactive Renin Secretion May Limit Its Effectiveness by Jean E. Sealey DSc and John H. Laragh MD. It appears in the May 2007 issue of the American Journal of Hypertension, Volume 20/Issue 5, published by Elsevier. (webwire.com)
  • A renin test is done to find the cause of high blood pressure (hypertension), especially when potassium levels in the blood are low. (wellspan.org)
  • Polyphenolic extract from Aronia melanocarpa reduce systolic and diastolic arterial tension values in rats with drug- induced hypertension, a phenomenon more pro nounced when polyphenols are associated with Aliskiren (renin inhibitor). (scirp.org)
  • Measurement of renin activity is useful in the differential diagnosis of individuals with hypertension. (spartanburgregional.com)
  • As a key player in the local renin-angiotensin system, (P)RR activation plays an important role in the development of cardiac fibrosis and proteinuria in hypertension and diabetes. (nih.gov)
  • Discovery of new renin inhibitors for treatment of hypertension is a promising area of research. (anaspec.com)
  • Inhibitors of the renin-angiotensin system (RASi), cornerstones of treatment of patients with hypertension and heart failure, have attracted attention as they may in theory influence the Ang-II level in COVID-19 and thereby the risk of ARDS [4,6] . (lww.com)
  • Collecting Duct Renin: A major player in Angiotensin II-dependent Hypertension. (biomedsearch.com)
  • Recently, the focus of interest on the role of the renin angiotensin system in the pathophysiology of hypertension has shifted towards greater emphasis on new developments in local renin angiotensin systems in specific tissues. (biomedsearch.com)
  • This brief review is focused on recent evidence that inappropriate activation of renin in distal nephron segments, by acting on angiotensinogen generated in the proximal tubule cells and delivered to the distal nephron may contribute to increased distal intrarenal angiotensin II formation, sodium retention and development and progression of hypertension. (biomedsearch.com)
  • 1. Patients with mild essential hypertension and elevated plasma renin activity, when compared with normal subjects and hypertensive subjects with normal plasma renin, demonstrated features of sympathetic nervous cardiovascular excitation, accompanied by a raised plasma noradrenaline concentration. (clinsci.org)
  • 2. An elevated heart rate at rest, shortened cardiac pre-ejection period, and greater heart rate reduction with acute β-adrenoreceptor blockade (intravenous propranolol) in high-renin essential hypertension were indicative of adrenergic cardiac excitation. (clinsci.org)
  • 4. These findings suggest that in mild high-renin essential hypertension increased adrenergic drive to the heart and resistance vessels exists. (clinsci.org)
  • In renal hypertension the activity of the renin-angiotensin system may be increased, normal, or depressed. (annals.org)
  • Reduction of renal mass by 70% is followed by suppressed renin activity and hypertension, which in the initial phase is caused by increased cardiac output. (annals.org)
  • In renal hypertensive rats negative sodium balance develops when blood pressure exceeds 180 mm Hg, resulting in high renin activity, which is the consequence and not the cause of hypertension. (annals.org)
  • GROSS F. The Renin-Angiotensin System and Hypertension. (annals.org)
  • To evaluate the efficacy and safety of renin inhibitors compared to ACE inhibitors in people with primary hypertension. (cochrane.org)
  • Plasma renin-guided therapeutics will improve systolic and diastolic blood pressure control in patients with untreated hypertension as well as in patients with treatment refractory or resistant hypertension that are managed by Clinical Hypertension Specialists. (clinicaltrials.gov)
  • Renin-guided therapeutics selection will reduce the total cost of antihypertensive care provided by Clinical Hypertension Specialists. (clinicaltrials.gov)
  • Williams, T.L., Elliott, J. and Syme, H.M. (2013), Renin-Angiotensin-Aldosterone System Activity in Hyperthyroid Cats with and without Concurrent Hypertension. (wiley.com)
  • Hypertension is caused by various factors and the predominant causes include an increase in cholesterol levels, incidence of diabetes, inconsistent modulation of renin and imbalanced sexual hormones. (mdpi.com)
  • High-renin hypertension is very common and for the most part, not indicative of anything different than if renin was not elevated. (ukidney.com)
  • Plasma renin activity (PRA) is measured as part of the diagnosis and treatment of hypertension (high blood pressure). (uclahealth.org)
  • Patients with essential hypertension may have renin and aldosterone levels checked to evaluate if they are salt-sensitive, which causes a low renin with normal aldosterone levels, and this helps to guide the physician in choosing the correct medication for these patients. (uclahealth.org)
  • Salt-sensitive patients with low renin hypertension respond well to diuretic medications. (uclahealth.org)
  • Chronic treatment with crude hog, or rat, renin administered subcutaneously to uninephrectomized rats elicits hypertension, renal and vascular lesions, hypertrophy of the zona glomerulosa of the adrenals, and renin depletion in the remaining kidney. (ahajournals.org)
  • Semipurified hog renin given in equipressor doses also causes renin depletion and stimulation of the zona glomerulosa, but no hypertension nor vascular disease. (ahajournals.org)
  • Thus, a prolonged and sustained resorption of renin seems to be a prerequisite for the development of hypertension. (ahajournals.org)
  • Since hypertension takes place only after a latent period during which arterial pressure remains within the normal range, it does not appear that hypertension can be attributed to the acute pressor effect of renin. (ahajournals.org)
  • It is proposed as a working hypothesis that renin, through angiotensin, initiates nervous mechanisms which are responsible for the development of benign hypertension and that the acute pressor effect of angiotensin is more specifically associated with the malignant phase of hypertension. (ahajournals.org)
  • Plasma renin then carries out the conversion of angiotensinogen , released by the liver, to angiotensin I . [2] Angiotensin I is subsequently converted to angiotensin II by the angiotensin-converting enzyme (ACE) found on the surface of vascular endothelial cells, predominantly those of the lungs. (wikipedia.org)
  • Renin cleaves a decapeptide from angiotensinogen , a globular protein . (wikipedia.org)
  • Renin can also be referred to as a hormone, as it has a receptor, the (pro)renin receptor, also known as the renin receptor and prorenin receptor (see also below), as well as enzymatic activity with which it hydrolyzes angiotensinogen to angiotensin I. The primary structure of renin precursor consists of 406 amino acids with a pre- and a pro-segment carrying 20 and 46 amino acids, respectively. (wikipedia.org)
  • The renin enzyme circulates in the bloodstream and hydrolyzes (breaks down) angiotensinogen secreted from the liver into the peptide angiotensin I. Angiotensin I is further cleaved in the lungs by endothelial-bound angiotensin-converting enzyme (ACE) into angiotensin II, the most vasoactive peptide. (wikipedia.org)
  • Renin activates the renin-angiotensin system by cleaving angiotensinogen, produced by the liver, to yield angiotensin I, which is further converted into angiotensin II by ACE, the angiotensin-converting enzyme primarily within the capillaries of the lungs. (wikipedia.org)
  • The (pro)renin receptor to which renin and prorenin bind is encoded by the gene ATP6ap2, ATPase H(+)-transporting lysosomal accessory protein 2, which results in a fourfold increase in the conversion of angiotensinogen to angiotensin I over that shown by soluble renin as well as non-hydrolytic activation of prorenin via a conformational change in prorenin which exposes the catalytic site to angiotensinogen substrate. (wikipedia.org)
  • This enzyme catalyses the following chemical reaction Cleavage of the Leu-Leu bond in synthetic renin substrate (horse), to produce angiotensin I, but not active on natural angiotensinogen This enzyme is present in submandibular glands of male mice. (wikipedia.org)
  • eng R01 DK072408 DK NIDDK NIH HHS United States Journal Article Comment 2017 02 09 England Hypertens Res 9307690 0916-9636 11002-13-4 Angiotensinogen 11128-99-7 Angiotensin II EC 3.4.23.15 Renin IM Hypertens Res. (tripdatabase.com)
  • Renin cleaves angiotensinogen to angiotensin I (Ang I), which is in turn converted by angiotensin-converting enzyme (ACE) to Ang II, the primary effector molecule of the RAS. (jci.org)
  • Renin cleaves an inactive peptide called angiotensinogen , converting it into angiotensin I . (bionity.com)
  • The renin acts on angiotensinogen to make AI. (physicsforums.com)
  • DABCYL-GABA-Ile-His-Pro-Phe-His-Leu-Val-Ile-His-Thr-EDANS (also called Renin Substrate I in some literature) contains a renin cleavage site that occurs in the N-terminal peptide of human angiotensinogen. (anaspec.com)
  • Cleavage of the substrate occurs specifically at the Leu-Val bond and corresponds to the renin cleavage site of angiotensinogen. (anaspec.com)
  • Through a series of chemical reactions, renin converts angiotensinogen (a protein released into the blood by the liver) to angiotensin I . As blood passes through the lungs, angiotensin I is converted into angiotensin II , a highly potent vasoconstrictor (an agent that induces narrowing of the blood vessels). (diabetesselfmanagement.com)
  • In the central nervous system, angiotensinogen is synthesized by astrocytes and subsequently cleaved by renin, angiotensin converting enzyme (ACE) and aminopeptidases or ACE2 and Neprilysin ( Bodiga and Bodiga, 2013 ). (frontiersin.org)
  • The circulating RAS comprises kidney-derived renin acting on liver-derived angiotensinogen to generate angiotensin (Ang) I that is converted to Ang II by angiotensin converting enzyme (ACE). (frontiersin.org)
  • However, tissues are the main site of production of angiotensin peptides by the circulating RAS, whereby plasma-derived renin acts on plasma-derived angiotensinogen to generate Ang I, which is converted to Ang II by endothelial ACE ( 1 - 4 ). (frontiersin.org)
  • Although many different concepts of local RAS have been described, a key feature is the local synthesis of RAS components including angiotensinogen and enzymes such as renin that cleave angiotensinogen to produce Ang peptides independently of the circulating RAS. (frontiersin.org)
  • This peptide is a renin substrate (angiotensinogen) labeled with EDANS/ DABCYL FRET pair for renin activity studies. (anaspec.com)
  • The renin in plasma is allowed to act on the plasma's endogenous substrate, angiotensinogen producing angiotensin I. This is measured by liquid chromatography/mass spectrometry (LC/MS-MS). (spartanburgregional.com)
  • Renin, a highly specific aspartyl protease, cleaves angiotensinogen, to yield angiotensin I. Angiotensin I is further converted into angiotensin II by ACE (Angiotensin Converting Enzyme). (anaspec.com)
  • Total RNA from a small part of the renal cortical biopsy specimens was reverse-transcribed, and the resultant cDNA was amplified for new major components of RAS (i.e., renin, renin receptor, angiotensinogen, ACE, ACE2, angiotensin II type 1 receptor, and angiotensin II type 2 receptor) and measured. (diabetesjournals.org)
  • Renin is a secreted endopeptidase that plays a crucial role in the regulation of blood pressure and salt balance through the cleavage of angiotensinogen, which is the only known physiological substrate of Renin. (rndsystems.com)
  • It is an aspartyl protease that cleaves angiotensinogen to form angiotensin I. In mouse, there are two genes that code for Renin. (rndsystems.com)
  • renin, secreted by the juxtaglomerular apparatus, activates the precursor angiotensinogen. (thefreedictionary.com)
  • Active renin mass concentration (ARC) is independent of the endogenous level of angiotensinogen, and less variable and more reproducible than plasma renin activity. (dovepress.com)
  • Renin converts angiotensinogen (a protein released into the blood by the liver) to angiotensin I. (uclahealth.org)
  • Whether it affects the use of renin - angiotensin -aldosterone system inhibitors and thereby negatively impacts outcome is unknown. (tripdatabase.com)
  • Blockade of the renin - angiotensin -aldosterone system (RAAS) with angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARB) has been shown to decrease incident atrial fibrillation (AF). (tripdatabase.com)
  • Renin - Angiotensin System Blockade Improves Cardiac Indices in Acromegaly Patients Blockade of the angiotensin-renin system , with angiotensin converting enzyme inhibitors (ACEi) and angiotensin receptor blockers (ARBs), has been shown to improve cardiac outcomes following myocardial infarction and delay progression of heart failure. (tripdatabase.com)
  • Design and preparation of potent, nonpeptidic, bioavailable renin inhibitors. (nih.gov)
  • Starting from known piperidine renin inhibitors, a new series of 3,9-diazabicyclo[3.3.1]nonene derivatives was rationally designed and prepared. (nih.gov)
  • Optimization of the positions 3, 6, and 7 of the diazabicyclonene template led to potent renin inhibitors. (nih.gov)
  • Renin inhibitors, for which aliskiren is a prototype, become the fourth class of drugs to lower blood pressure by blocking the renin-angiotensin system. (webwire.com)
  • The SensoLyte 520 Mouse Renin Assay Kit provides a convenient assay for high throughput screening of renin inhibitors and for continuous assay of mouse renin activity using a 5-FAM/QXL 520 FRET peptide. (anaspec.com)
  • Inhibitors of the system are beneficial in treating these pathologies and include direct renin inhibitors, angiotensin-converting enzyme inhibitors, and angiotensin receptor antagonists. (springer.com)
  • Influence of inhibitors of the renin-angiotensin system on r. (lww.com)
  • These include three types of renin-angiotensin system (RAS) inhibitors: angiotensin converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs) and renin inhibitors. (cochrane.org)
  • Direct renin inhibitors block the enzyme renin from triggering a process that helps regulate blood pressure. (peacehealth.org)
  • Direct renin inhibitors, angiotensin-converting enzyme (ACE) inhibitors, and angiotensin II receptor blockers (ARBs) all target the same process that narrows blood vessels. (peacehealth.org)
  • Direct renin inhibitors are used to lower high blood pressure . (peacehealth.org)
  • Direct renin inhibitors can lower blood pressure. (peacehealth.org)
  • Direct renin inhibitors are a newer type of medicine for high blood pressure. (peacehealth.org)
  • Renin inhibitors inhibit the enzyme renin, which results in widening blood vessels, making it easier for the blood to flow, which lowers blood pressure. (healthy-ojas.com)
  • Who should avoid renin inhibitors? (healthy-ojas.com)
  • Avoid Renin inhibitors, if you are pregnant or planning for pregnancy or have kidney problems. (healthy-ojas.com)
  • What are the side effects of renin inhibitors? (healthy-ojas.com)
  • This is the most direct causal link between blood pressure and renin secretion (the other two methods operate via longer pathways). (wikipedia.org)
  • Human renin is secreted by at least 2 cellular pathways: a constitutive pathway for the secretion of the precursor prorenin and a regulated pathway for the secretion of mature renin. (wikipedia.org)
  • Renin secretion is also stimulated by sympathetic nervous stimulation, mainly through β1 adrenoreceptor activation. (wikipedia.org)
  • Control of Renin Synthesis and Secretion. (biomedsearch.com)
  • Longer lasting challenges of renin secretion lead to changes in the number of renin-producing cells, which occur by a metaplastic transformation of renin cell precursors such as preglomerular vascular smooth muscle or extraglomerular mesangial cells. (biomedsearch.com)
  • Beta-blockers lower blood pressure by blocking the effects of adrenaline (also called epinephrine ), a hormone that increases heart rate and contractility, and inhibiting renin secretion by the kidney. (diabetesselfmanagement.com)
  • In 8 patients, renal venous PRA was higher than arterial PRA, indicating the renal secretion of renin into the circulation. (annals.org)
  • Secretion of renin from JG cells at the organ level is controlled by the four main mechanisms: the sympathetic nervous system, the local JG apparatus baroreflex, the macula densa mechanism, and several hormones acting locally within the JG apparatus. (kegg.jp)
  • Renin secretion at the level of renal JG cells appears to be controlled mainly by classic second messengers, namely cAMP, cGMP, and free cytosolic calcium concentration. (kegg.jp)
  • angiotension II also stimulates aldosterone secretion, which causes sodium retention, an increase in blood pressure, and restoration of renal perfusion, which shuts off the signal for renin release (negative feedback). (thefreedictionary.com)
  • Transfection and in vitro studies confirmed that both mutations affect ER translocation and processing of nascent preprorenin, resulting either in reduced (p.Leu16del) or abolished (p.Leu16Arg) prorenin and renin biosynthesis and secretion. (sigmaaldrich.com)
  • In all three groups, baseline renal plasma flow (RPF) was positively correlated with the RPF response to blocking the renin-angiotensin system (RAS). (diabetesjournals.org)
  • Somewhat to our surprise, we found that baseline renal plasma flow (RPF) and glomerular filtration rate were highly and positively correlated with the renal hemodynamic response to blocking the renin-angiotensin system (RAS) with irbesartan in patients with type 2 diabetes and nephropathy ( Fig. 1 ). (diabetesjournals.org)
  • These include the (pro)renin receptor ( 5 ), renin-independent mechanisms of Ang peptide generation from Ang- (1-12) ( 6 ), intracellular (or intracrine) RAS that may contribute to cardiovascular disease ( 7 , 8 ), and AT2 receptors ( 7 ) and the ACE2/Ang-(1-7)/Mas receptor pathway ( 6 - 8 ) that may mediate therapeutic benefit in cardiovascular disease. (frontiersin.org)
  • In the present study, we investigated the role of liver X receptor α (LXRα) and LXRβ in the regulation of renin. (jci.org)
  • Pro)renin Receptor: A Treatment Target for Diabetic Retinopathy? (diabetesjournals.org)
  • The (pro)renin receptor ((P)RR) is a unique molecule that binds prorenin and renin in tissues, not only leading to their activation, but also inducing intracellular signaling. (nih.gov)
  • This will be the first study to assess vitamin D receptor (VDR) biological (PRA, PRC, renin mRNA, and polymorphisms) and hypertensive activity in patients without vitamin D deficiency. (clinicaltrials.gov)
  • Furthermore, new major components for RAS, renin receptor (RER) ( 16 ), and ACE2 ( 17 ) have emerged recently. (diabetesjournals.org)
  • BML-111, a lipoxin receptor agonist, protects against acute injury via regulating the renin angiotensin-aldosterone system. (annals.org)
  • Soluble (Pro)renin Receptor and Obstructive Sleep Apnea Syndrome: Oxidative Stress in Brain? (mdpi.com)
  • Pro)renin receptor ((P)RR) is a multi-functional molecule that is related to both the renin-angiotensin system (RAS) and vacuolar H + -ATPase (v-ATPase), an ATP-dependent multi-subunit proton pump. (mdpi.com)
  • A high renin value can mean kidney disease, blockage of an artery leading to a kidney, Addison's disease , cirrhosis , excessive bleeding (hemorrhage), or hypertensive emergency is present. (wellspan.org)
  • Home Resources Ask the Experts For Professionals General Nephrology Questions Worried of High Renin Res. (ukidney.com)
  • This fluorogenic peptide substrate is used to continuously measure the proteolytic activity of human renin. (anaspec.com)
  • Cleavage of the substrate by renin liberates the peptidyl-EDANS fragment from proximity with the DABCYL acceptor, restoring the fluorescence of the EDANS moiety. (anaspec.com)
  • The kinetics of renin-catalyzed hydrolysis of this substrate is shown to be consistent with a simple substrate inhibition model with a substrate Km approximately equal to 1.5 mM at physiological pH. (anaspec.com)
  • The substrate can detect renin as low as 30 ng/mL after an incubation of only 3-5 min. (anaspec.com)
  • The kit contains: 5-FAM/QXL 520-based FRET mouse specific renin substrate (Ex/Em=490/520 nm upon cleavage), assay buffer, mouse recombinant prorenin, reagents for conversion of prorenin to renin, inhibitor, fluorescence reference standard for calibration, and an optimized assay protocol. (anaspec.com)
  • 1. A synthetic 3-([ 14 C]valine)-labelled tetradecapeptide renin substrate was used to measure renin concentration. (biochemj.org)
  • Renin liberated 14 C-labelled angiotensin I, which was separated from the labelled substrate by paper chromatography. (biochemj.org)
  • 2. The rate of conversion of the substrate into angiotensin I was shown to be linearly related to renin concentration and time under suitable conditions. (biochemj.org)
  • 3. It is suggested that the use of a pure substrate offers advantages that include the standardization of current units of renin measurement. (biochemj.org)
  • renin substrate is a topic covered in the Taber's Medical Dictionary . (tabers.com)
  • Taber's Online , www.tabers.com/tabersonline/view/Tabers-Dictionary/730457/all/renin_substrate. (tabers.com)
  • Combination therapy also proved unsafe in the ALTITUDE trial, which tested the direct renin inhibitor aliskiren in addition to an ACE inhibitor or an ARB. (forbes.com)
  • A new drug called Aliskiren is being released in 2007 which directly inhibits renin. (bionity.com)
  • Aliskiren (Tekturna , Rasilez ) is the first of a new class of orally active antihypertensive drugs that works by inhibiting renin. (webwire.com)
  • Treatment with the renin inhibitor aliskiren, the angiotensin II converting-enzyme inhibitor enalapril, as well as preventive or therapeutic application of the AT1R antagonist losartan, resulted in a significantly ameliorated course of MOG-EAE. (pnas.org)
  • When given with an ACEI or ARB, aliskiren produces significant additional BP reduction indicative of complimentary pharmacology and more complete renin-angiotensin system blockade. (dovepress.com)
  • It has been theorized that dual blockade of the renin-angiotensin-aldosterone system (RAAS) might prove even more beneficial, but these hopes have not been realized. (forbes.com)
  • What is the role of renin-angiotensin blockade in the treatment of immunoglobulin A (IgA) nephropathy? (medscape.com)
  • OBJECTIVE -Recent studies have proved that blockade of the renin-angiotensin system (RAS) retards the progression of diabetic nephropathy, whereas hyporeninemia is known as a typical state in diabetic subjects. (diabetesjournals.org)
  • 3. Blood pressure was normalized by 'total' autonomic blockade (atropine plus propranolol plus phentolamine) in the hypertensive subjects with elevated plasma renin activity. (clinsci.org)
  • Only renin-expressing cells in the kidney are capable of generating active renin from prorenin, which is stored in prominent vesicles and which is released into the circulation upon demand. (biomedsearch.com)
  • Here, we measured plasma levels of active renin and aldosterone in patients referred for cardiac catheterization in order to determine the prevalence of elevated renin, aldosterone, and the aldosterone-renin ratio. (ovid.com)
  • A chemiluminescence assay was used to measure plasma aldosterone concentration (PAC) and active renin levels in 833 consecutive patients, after an overnight fasting and without any medication for least 12 hours. (ovid.com)
  • Plasma renin levels were also measured in 116 treated hypertensive patients. (bmj.com)
  • It is concluded that levels of plasma renin are not a reliable index of the probability of hypertensive patients suffering a stroke or myocardial infarction. (bmj.com)
  • Compare plasma renin activity (PRA) and plasma renin concentration (PRC) in hypertensive patients (JNC VII stage I) following 14 days treatment with calcitriol (1α, 25-[OH]2 vitamin D3) or matched placebo. (clinicaltrials.gov)
  • Renin Angiotensin Activity in 100 Hypertensive Patients. (annals.org)
  • The renin-angiotensin system ( RAS ) or the renin-angiotensin-aldosterone system ( RAAS ) is a hormone system that regulates blood pressure and fluid balance . (wikipedia.org)
  • Renin (etymology and pronunciation), also known as an angiotensinogenase, is an aspartic protease protein and enzyme secreted by the kidneys that participates in the body's renin-angiotensin-aldosterone system (RAAS)-also known as the renin-angiotensin-aldosterone axis-that mediates the volume of extracellular fluid (blood plasma, lymph and interstitial fluid) and arterial vasoconstriction. (wikipedia.org)
  • The renin-angiotensin system (RAS) or the renin-angiotensin-aldosterone system (RAAS) is a hormone system that helps regulate long-term blood pressure and extracellular volume in the body. (bionity.com)
  • 3 Since then, expansion of the RAS to the renin-angiotensin-aldosterone (RAAS) system and discovery of several bioactive peptides produced through Ang-II degradation has contributed to the increasing complexity of the RAS ( Figure ), and the search continues. (ahajournals.org)
  • The aspartyl protease renin is the rate limiting activity of the renin-angiotensin-aldosterone system (RAAS). (biomedsearch.com)
  • The Gordon Research Conference "Angiotensin" is a prestigious scientific congress, bringing together researchers and scientific experts from around the world, where the latest discoveries and advances in the field of the renin angiotensin aldosterone system (RAAS) are presented. (yahoo.com)
  • Many studies suggested inhibition of renin-angiotensin-aldosterone system (RAAS) could reduce new AF in various clinical conditions. (bmj.com)
  • The renin-angiotensin-aldosterone system (RAAS) is crucial to the homeostasis of both the cardiovascular and respiratory systems. (ersjournals.com)
  • Importantly, SARS-CoV-2 utilises and interrupts this pathway directly, which could be described as the renin-angiotensin-aldosterone-SARS-CoV (RAAS-SCoV) axis. (ersjournals.com)
  • When renal blood flow is reduced, juxtaglomerular cells in the kidneys convert the precursor prorenin (already present in the blood) into renin and secrete it directly into circulation . (wikipedia.org)
  • This article describes investigations of several aspects of the molecular biology of the human renin gene and the three-dimensional structure of renin and its precursor, prorenin. (nih.gov)
  • The primary structure of human renin precursor has been deduced from its cDNA sequence. (pnas.org)
  • The amino acid sequence predicted from the cDNA sequence shows that the human renin precursor consists of 406 amino acids with a pre and a pro segment carrying 20 and 46 amino acids, respectively. (pnas.org)
  • Before you take a direct renin inhibitor, tell your doctor about any other medicines you take and any other health problems you have. (peacehealth.org)
  • Some studies have shown an association between increased renin activity and a cluster of cardiovascular disease risk factors called Syndrome X , or metabolic syndrome. (diabetesselfmanagement.com)
  • Background and Purpose- Our objective was to investigate the associations between polymorphisms in representative genes of the renin angiotensin system with measures of cerebral blood flow regulation in older adults. (ahajournals.org)
  • 11 Therefore, we hypothesized that polymorphisms in genes of the renin angiotensin system are also associated with autoregulation and the cerebrovascular response to changes in CO 2 . (ahajournals.org)
  • As the rate-limiting protease that catalyzes the initial step in the activation of the renin angiotensin system (RAS) proteolytic cascade, renin is a master regulator of blood pressure and fluid homeostasis. (jci.org)
  • Activation of the renin-angiotensin system (RAS) by high glucose, mechanical stress, and proteinuria has been implicated in the major changes associated with diabetic nephropathy ( 4 ). (diabetesjournals.org)
  • A blood sample required for measurement of plasma aldosterone and/or renin levels is taken by needle from a vein in the arm. (labtestsonline.org.uk)
  • 1. The effect of endogenous sympathetic stimulation (induced by urinary bladder stimulation) and intravenous infusion of noradrenaline and isoprenaline on blood pressure, heart rate and levels of plasma renin activity and plasma aldosterone were studied in six tetraplegic patients. (clinsci.org)
  • 2. Bladder stimulation in the tetraplegic patients caused a marked rise in blood pressure and fall in heart rate, but no change in plasma renin activity or plasma aldosterone. (clinsci.org)
  • Plasma renin activity and plasma aldosterone did not change in either group. (clinsci.org)
  • Comparative Analysis of Renin - Angiotensin System (RAS)-Related Gene Expression Between Hypertensive and Normotensive Rats BACKGROUND The renal renin - angiotensin system (RAS) is physiologically important for blood pressure regulation. (tripdatabase.com)
  • In male but not female hypoxia-exposed offspring, renal renin mRNA was increased at weaning. (nature.com)
  • By 12 months, renal renin mRNA expression and concentrations were elevated in both sexes. (nature.com)
  • Renal Renin (Renin-1) is synthesized as a 381 aa proform (aa 22 - 402). (rndsystems.com)
  • In the latter condition, however, the normal renin activity corresponds to a relative increase, since after unilateral nephrectomy plasma renin activity and renal renin decrease. (annals.org)
  • The library was screened for human renin sequences by hybridization with the previously cloned mouse renin cDNA. (pnas.org)
  • Mouse Renin is a secreted, 42 - 47 kDa glycosylated member of the peptidase A1 family. (rndsystems.com)
  • If the perfusion of the juxtaglomerular apparatus in the kidney's macula densa decreases, then the juxtaglomerular cells (granular cells, modified pericytes in the glomerular capillary) release the enzyme renin . (wikipedia.org)
  • The enzyme renin is secreted by pericytes (mural cells) (1) in the vicinity of the afferent arterioles and similar microvessels of the kidney from specialized cells of the juxtaglomerular apparatus-the juxtaglomerular cells, in response to three stimuli: A decrease in arterial blood pressure (that could be related to a decrease in blood volume) as detected by baroreceptors (pressure-sensitive cells). (wikipedia.org)
  • If the perfusion of the juxtaglomerular apparatus in the kidneys decreases, then the juxtaglomerular cells release the enzyme renin . (bionity.com)
  • Aldosterone/renin ratio 172.0. (medhelp.org)
  • The results were: Aldosterone 17.2, Renin 0.1, Aldosterone/Renin Ratio 172.0. (medhelp.org)
  • I don't know a lot about the Aldosterone/Renin Ratio, but did notice on the lab report that the results were flagged 'high' and anything above 25 is suggestive of hyperaldosteronism. (medhelp.org)
  • This is the first time he's ordered the Aldosterone/Renin Activity Ratio, so may we're on to something! (medhelp.org)
  • This prospective study of consecutive cardiac disease patients referred for cardiac catheterization has revealed distinct cardiac disease condition-associated differences in the frequencies of elevations in plasma renin, PAC, and the aldosterone-renin ratio. (ovid.com)
  • Association of seven renin angiotensin system gene polymorphisms with restenosis in patients following coronary stenting Percutaneous coronary intervention, despite being effective for coronary revascularization, causes in-stent restenosis due to neointimal hyperplasia in a large number of patients. (tripdatabase.com)
  • Molecular biology of human renin and its gene. (nih.gov)
  • The renin gene was found to be expressed significantly in the renal juxtaglomerular cells and several other cell types. (nih.gov)
  • Cultured human uterine-placental cells expressed the human renin gene at levels higher than in other cell types assessed. (nih.gov)
  • By contrast, cAMP induces in essence gene activation in WI26VA4 transformed human lung fibroblasts in which renin mRNA levels increase by up to 150-fold in response to forskolin. (nih.gov)
  • Thus, cAMP may activate renin gene expression under certain circumstances and tissue-specific renin gene expression may be directed by more than one mechanism. (nih.gov)
  • Renin is an aspartyl protease that raises blood pressure, retains sodium, and alters gene transcription to adversely affect the kidney and heart. (springer.com)
  • CONCLUSIONS -The results suggest that renal tissue RAS might be activated in the respect that ACE gene expression is upregulated in spite of a tendency to low renin expression in type 2 diabetic nephropathy. (diabetesjournals.org)
  • To test for a possible role of angiotensin II in the developmental deactivation of renin expression, we studied the development of intrarenal renin expression in mice lacking ANG II AT1a, AT1b, or AT2 receptors and in animals with abolished circulating ANG II due to deletion of the gene for angiotensin I-converting enzyme (ACE). (unboundmedicine.com)
  • Morris BJ: New possibilities for intracellular renin and inactive renin now that the structure of the human renin gene has been elucidated. (hmdb.ca)
  • We studied the expression of kidney renin gene in hypertensive animals by measuring the kidney renin messenger (m) RNA. (ovid.com)
  • Propranolol had no effect on the kidney renin gene expression in either WKY or SHR. (ovid.com)
  • These results indicate that SHR show an enhanced expression of the renin gene in the kidney compared with WKY in response to stimuli that increase renin release. (ovid.com)
  • Further, renin angiotensin system gene polymorphisms are associated with angiotensin II levels and measures of systemic blood pressure regulation 10 and baroreflex sensitivity. (ahajournals.org)
  • Dominant renin gene mutations associated with early-onset hyperuricemia, anemia, and chronic kidney failure. (sigmaaldrich.com)
  • Through linkage analysis and candidate gene sequencing, we identified three unrelated families with the autosomal-dominant inheritance of early onset anemia, hypouricosuric hyperuricemia, progressive kidney failure, and mutations resulting either in the deletion (p.Leu16del) or the amino acid exchange (p.Leu16Arg) of a single leucine residue in the signal sequence of renin. (sigmaaldrich.com)
  • 1993). A continuous fluorescence assay of renin activity. (anaspec.com)
  • This assay recognizes both the Pro- and mature versions of recombinant human Renin. (rndsystems.com)
  • The recovery of Renin spiked to levels throughout the range of the assay in various matrices was evaluated. (rndsystems.com)
  • To assess the linearity of the assay, samples containing and/or spiked with high concentrations of Renin were serially diluted with Calibrator Diluent to produce samples with values within the dynamic range of the assay. (rndsystems.com)
  • Renin Inhibition - a Feasible Clinical Therapy? (portlandpress.com)
  • There are reasons to speculate that renin inhibition might prove to be a superior strategy for blocking the renin-angiotensin-aldosterone system compared with ACEIs or ARBs. (dovepress.com)
  • We hypothesize that vitamin D inhibition of renin transcription will produce significant reductions in PRA, PRC, renin transcription, inflammatory cytokines, SBP, and DBP, with potential variation by VDR genotype. (clinicaltrials.gov)
  • The most prominent renin super-enhancer may act as a chromatin sensor of signals that convey the physiologic status of the organism, and is responsible for the transformation of renin cell descendants to the renin phenotype, a fundamental process to ensure homeostasis. (jci.org)
  • Renin is a hormone made by the kidneys. (medlineplus.gov)
  • The kidneys of the rats in the 500ppm Pb treated group had elevated renin concentrations. (cdc.gov)
  • The renin-angiotensin system is thought to be important in adaptations to low-salt diets and normal development of the kidneys in utero. (springer.com)
  • Although the number of renin-expressing cells declined during final maturation of the kidneys, the atypical distribution pattern of renin cells was maintained. (unboundmedicine.com)
  • During postnatal maturation of mouse kidneys, interruption of the RAS causes severe hyperplasia of renin cells via a mechanism that centrally involves AT(1a) receptors. (unboundmedicine.com)
  • However, the distribution pattern of renin cells in adult kidneys with an interrupted RAS does not mimic any normal developmental stage since renin expression is frequently found in cells outside the arteriolar vessel walls in RAS mutants. (unboundmedicine.com)
  • Renin, produced by the kidney, stimulates production of angiotensin II in the bloodstream. (labtestsonline.org.uk)
  • While cAMP generally stimulates renin release and the intracellular calcium concentration suppresses the exocytosis of renin, the effects of cGMP in the regulation of the renin system are more complex as it both may stimulate or inhibit renin release. (kegg.jp)
  • Untreated LXRβ-/- mice exhibited reduced kidney renin mRNA levels compared with controls. (jci.org)
  • The kidney renin mRNA was quantified by densitometric Northern biot analysis using a 32 P-labelled rat renin genomic DNA fragment as a hybridization probe. (ovid.com)
  • Both sodium depletion and captopril treatment caused significant increases in the kidney renin mRNA in SHR and WKY. (ovid.com)
  • The aspartyl-protease renin is the key regulator of the renin-angiotensin-aldosterone system, which is critically involved in extracellular fluid volume and blood pressure homeostasis of the body. (kegg.jp)
  • The Local Cardiac Renin-Angiotensin Aldosterone System, Second Edition updates new findings on the local renin-angiotensin systems (RAS) with a focus on the local RAASs of the cardiovascular system and kidney. (springer.com)
  • The concept of a "local" renin angiotensin system (RAS) can mean different things to different people. (frontiersin.org)
  • My thinking for this is that renin and aldosterone control sodium and potassium, so I was thinking they would have to be somewhat off for the ratio to be off like that. (medhelp.org)
  • My aldosterone is normal so as with my aldosterone and renin ratio is normal. (ukidney.com)
  • Reference values for the aldosterone-to-renin ratio (ARR) using ARC are still undefined. (dovepress.com)
  • The angiotensin-renin ratio was elevated in AF patients and in patients with hypertensive cardiomyopathy. (ovid.com)
  • 2. The pressor response to renin in brief experiments is independent of the height of the arterial pressure or the presence of the suprarenals. (rupress.org)
  • 6. Continuous infusion of renin produces a prolonged rise of arterial pressure in normal and chronically suprarenalectomized dogs, but the pressure ultimately falls despite continued infusion. (rupress.org)
  • This test measures the level of renin in the blood. (medlineplus.gov)
  • The level of renin mRNA appears to be modulated by the binding of HADHB, HuR and CP1 to a regulatory region in the 3' UTR. (wikipedia.org)
  • Using renin cells at various stages of stimulation, we identified regions in the genome where the chromatin is open for transcription, mapped histone modifications characteristic of active enhancers such as H3K27ac, and tracked deposition of transcriptional activators such as Med1, whose deletion results in ablation of renin expression and low blood pressure. (jci.org)
  • In LXRα-/- mice, the elevation of renin triggered by adrenergic stimulation was abolished. (jci.org)
  • 3. There is no parallelism between the pressor responses to carotid sinus stimulation, adrenine, and tyramine on the one hand and renin on the other. (rupress.org)
  • 5. We conclude that in tetraplegic patients neither endogenous sympathetic stimulation by bladder stimulation nor infusion of noradrenaline raises plasma renin activity. (clinsci.org)
  • Angiotensin II is the major bioactive product of the renin-angiotensin system, binding to receptors on intraglomerular mesangial cells , causing these cells to contract along with the blood vessels surrounding them and causing the release of aldosterone from the zona glomerulosa in the adrenal cortex . (wikipedia.org)
  • Renin is secreted from juxtaglomerular kidney cells, which sense changes in renal perfusion pressure, via stretch receptors in the vascular walls. (wikipedia.org)
  • 2 It took 7 more decades of basic, translational, and clinical research to discover the pressor effect of renal extracts (ascribed to renin) in 1898 and another 10 decades of imaginative work by many to culminate in the discovery of angiotensin II (Ang-II), the primary effector peptide of the RAS, and its receptors (AT 1 R and AT 2 R) in 2000. (ahajournals.org)
  • The renin-angiotensin system (RAS), acting through type 1 angiotensin (AT1) receptors, is a master regulator of fluid homeostasis. (anaspec.com)
  • Angiotensin II interacts with AT1 receptors to mediate most renin effects. (springer.com)
  • The development of intrarenal renin expression was normal in mice lacking ANG II AT1b or AT2 receptors. (unboundmedicine.com)
  • In animals lacking both ANG II AT1a and AT1b receptors, ACE, or ANG II AT1a receptors, renin expression was normal early and renin disappeared from mature vessels until development of cortical interlobular and afferent arterioles began. (unboundmedicine.com)
  • Renin/prorenin receptors. (wikipathways.org)
  • Transfected renin promoters showed cell type-specific expression and cAMP responsiveness in these cells in constructs containing as few as 102 bp of 5'-flanking DNA. (nih.gov)
  • In conclusion, we show herein that LXRα and LXRβ regulate renin expression in vivo by directly interacting with the renin promoter and that the cAMP/LXRα signaling pathway is required for the adrenergic control of the renin-angiotensin system. (jci.org)
  • During nephrogenesis, renin expression shifts from the vessel walls of interlobular arteries to the terminal portions of afferent arterioles in a wavelike pattern. (unboundmedicine.com)
  • Since the mechanisms responsible for the developmental deactivation of renin expression are as yet unknown, we hypothesized that the developing renin-angiotensin system (RAS) may downregulate itself via negative feedback to prevent overactivity of renin. (unboundmedicine.com)
  • These findings suggest that ANG II does not play a central role in the typical developmental shift in renin expression from the arcuate vessels to the afferent arterioles. (unboundmedicine.com)
  • The present study sought to assess the cellular source, spatial distribution and temporal response of renin expression and synthesis in the rat heart following anterior transmural MI, and to determine its relationship to circulating renin activity. (unboundmedicine.com)
  • Thus, renin expression and activity appear at sites of repair in the infarcted rat heart on day 3 and rise progressively thereafter over 4 weeks, independent of circulating renin. (unboundmedicine.com)
  • TY - JOUR T1 - Renin expression at sites of repair in the infarcted rat heart. (unboundmedicine.com)
  • Effect of apocynin treatment on renal expression of COX-2, NOS1, and renin in Wistar-Kyoto and spontaneously hypertensive rats. (wikipathways.org)
  • The high plasma renin activity is seen as an expression of sympathetic nervous system overactivity. (clinsci.org)
  • Expression of renin and other components of the renin-angiotensin system was decreased accordingly in kidney biopsy specimens from affected individuals. (sigmaaldrich.com)
  • It is likely that expression of the mutant proteins has a dominant toxic effect gradually reducing the viability of renin-expressing cells. (sigmaaldrich.com)
  • This control involves regulation at the transcriptional level, folding of prorenin, sorting of prorenin to a regulated pathway where it is proteolytically cleaved to renin and released in response to secretogogues, constitutive release of uncleaved prorenin, and nonproteolytic activation of prorenin. (nih.gov)
  • 4. The biosynthetic pathway for renin was established by continuous-labelling, pulse-chase and cell-free translation studies of submandibular gland tissue from normal and testosterone-induced mice. (portlandpress.com)
  • a selective regulator of the aldosterone biosynthetic pathway that acts by increasing aldosterone production and sodium retention as a result of volume depletion, with resulting increased renin production in the kidney and conversion of angiotensin I in the plasma to angiotensin II. (thefreedictionary.com)
  • You may need a renin test if you've been diagnosed with high blood pressure, especially if it doesn't respond well to standard blood pressure medicines . (medlineplus.gov)
  • Be aware that renin level can be affected by pregnancy, as well as the time of day and the body position when blood is drawn. (ucsfhealth.org)
  • Renin is a protein ( enzyme ) released by special kidney cells when you have a decreased salt (sodium) level or low blood volume. (ucsfhealth.org)
  • Most often, the renin blood test is done at the same time as an aldosterone blood test to calculate the renin to aldosterone level. (ucsfhealth.org)
  • If you have high blood pressure , your doctor may order a renin and aldosterone test to help determine the cause of your elevated blood pressure. (ucsfhealth.org)
  • Renin cells are crucial for survival - they control fluid-electrolyte and blood pressure homeostasis, vascular development, regeneration, and oxygen delivery to tissues. (jci.org)
  • Renin-expressing cells have been conserved through evolution and maintain blood pressure and fluid homeostasis. (jci.org)
  • The renin-angiotensin system is often manipulated clinically to treat high blood pressure . (bionity.com)
  • Renin levels are high in the fetus, while angiotensin II levels are significantly lower - this is due to the limited pulmonary blood flow, preventing ACE (found predominantly in the pulmonary circulation) from having its maximum effect. (bionity.com)
  • Though renin itself has no effect on blood pressure, angiotensin II does. (diabetesselfmanagement.com)
  • Renin Angiotensin System (RAS) is a hormonal system that regulates blood pressure and fluid balance through a coordinated action of renal, cardiovascular, and central nervous systems. (frontiersin.org)
  • Their reactive renin responses might be so great as to induce a rise in blood pressure. (webwire.com)
  • The renin-angiotensin-aldosterone system controls blood pressure and salt-volume homeostasis. (jci.org)
  • Blood samples were obtained at 75 and 90 minutes for determination of BSP and renin. (cdc.gov)
  • Renin works with aldosterone (a hormone made by the adrenal glands ) and several other substances to help balance sodium and potassium levels in the blood and fluid levels in the body, which affects your blood pressure. (wellspan.org)
  • In some people, it may be normal to have high blood levels of both renin and aldosterone. (wellspan.org)
  • The purpose of the study was to emphasize the effects of the association between the renin inhibitor and the polyphenolic extract on biochemical parameters and systolic and diastolic blood pressure. (scirp.org)
  • The increase in blood pressure in these rats was blocked by administration of renin-angiotensin system (RAS) blockers or by reduction of uric acid with allopurinol.9 More recently, febuxostat was also shown effective in this experimental model.10 Febuxostat was recently approved by the FDA as Uloric. (clinicaltrials.gov)
  • 5. Intracisternal injection of renin elicits no significant rise in blood pressure or other circulatory manifestations. (rupress.org)
  • 7. Tachyphylaxis develops in the isolated rabbit's ear perfused with blood and small doses of renin. (rupress.org)
  • The same blood perfused through a second ear causes no vasoconstriction when renin is added. (rupress.org)
  • 9. Blood from animals made tachyphylactic by repeated injections of renin is lacking in activator and also fails to cause vasoconstriction in the rabbit's ear when renin and renin-activator are added. (rupress.org)
  • Blood pressure may fall after a period of renin infusion despite the pressure in the blood of excess renin. (rupress.org)
  • We propose to directly measure the effect of vitamin D therapy on plasma renin activity (PRA), plasma renin concentration (PRC), renin transcription (in mononuclear leukocytes), and blood pressure in hypertensive (but otherwise healthy) patients in a randomized, controlled, experimental trial. (clinicaltrials.gov)
  • Renin is an enzyme released by specialized cells of the kidney into the blood. (uclahealth.org)
  • Intrarenal renin - angiotensin system activation in end-stage renal disease. (tripdatabase.com)
  • This alters the intrarenal renin-angiotensin system and the juxtaglomerular apparatus functionality and leads to nephron dropout and progressive kidney failure. (sigmaaldrich.com)
  • Renin levels were not significantly different in patients with or without vascular complications. (bmj.com)
  • There was no relation between plasma renin level and vascular complications. (bmj.com)
  • Anti-leech renin stains the vascular pole of the glomerulus and the afferent arteriole of the rat kidney. (nel.edu)
  • Patients with secondary hyperaldosteronism (that is, caused by kidney disease or renal vascular disease) will have increased plasma levels of renin and aldosterone. (uclahealth.org)
  • It can also be activated by a decrease in the filtrate sodium chloride (NaCl) concentration or a decreased filtrate flow rate that will stimulate the macula densa to signal the juxtaglomerular cells to release renin. (wikipedia.org)
  • The macula densa senses changes in sodium delivery to the distal tubule, and responds to a drop in tubular sodium load by stimulating renin release in the juxtaglomerular cells. (wikipedia.org)
  • Plasma renin levels, measured in 39 untreated patients in 1967, under conditions of sodium loading and sodium depletion have been related to the incidence of stroke and myocardial infarction. (bmj.com)
  • Your doctor will tell you if you should change the amount of sodium (salt) you ingest in your diet, your use of diuretics or other medications, or your exercise routine before aldosterone and renin are tested. (labtestsonline.org.uk)
  • In the fetus , the renin-angiotensin system is predominantly a sodium-losing system, as angiotensin II has little or no effect on aldosterone levels. (bionity.com)
  • For 3 days before a renin test, you may be asked to follow a special low-sodium diet. (wellspan.org)
  • Dietary sodium levels during the period prior to testing can affect renin levels. (spartanburgregional.com)
  • Plasma renin activity (PRA) in SHR and WKY was increased similarly by sodium depletion and by treatment with captopril. (ovid.com)
  • Lack of availability of tools to study the specifics of renin regulation has limited advances in this field. (jci.org)
  • Quantitative RT-PCR analyses showed an up-regulation of renin, angiotensin-converting enzyme, as well as AT1R in the inflamed spinal cord and the immune system, including antigen presenting cells (APC). (pnas.org)
  • LXRα-/-LXRβ-/- mice showed a combined phenotype of lower basal renin and blunted adrenergic response. (jci.org)
  • Studies with transfected vectors expressing a mutant cAMP-responsive protein kinase A regulatory subunit suggest that cAMP is not responsible for basal renin promoter activity in the placental cells. (nih.gov)
  • The purpose of this study is the measure renin, angiotensin, and aldosterone activity, as well as other hormonal axes, in people with and without HIV infection, and with and without increased belly fat. (clinicaltrials.gov)
  • The juxtaglomerular cells are also stimulated to release renin by signaling from the macula densa. (wikipedia.org)
  • Our efforts led to the discovery of compound (+)-26g that inhibits renin with an IC(50) of 0.20 nM in buffer and 19 nM in plasma. (nih.gov)
  • When there is a threat to survival, those descendants are transformed and reenact the renin phenotype to restore homeostasis. (jci.org)
  • The renin super-enhancers play a key role in the molecular memory of renin cell function, a mechanism at the core of preserving homeostasis. (jci.org)