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.

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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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 - ...
... is not commonly referred to as a hormone, albeit it having a receptor, the (pro)renin receptor, also known as the renin ... 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 ...
"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) Portal: Biology (EC 3.4.21). ... Drinkwater CC, Evans BA, Richards RI (June 1988). "Sequence and expression of mouse gamma-renin". The Journal of Biological ...
... s bind to the active site of renin and inhibit the binding of renin to angiotensinogen, which is the rate- ... Brown, M. J. (2006). "Direct renin inhibition - a new way of targeting the renin system". Journal of the Renin-Angiotensin- ... Consequently, renin inhibitors prevent the formation of Ang I and Ang II. Renin inhibitors may also prevent Ang-(1-7), Ang-(1-9 ... Renin is a circulating enzyme that acts on a circulating peptide, angiotensinogen. Renin cleaves the peptide at the Leu10-Val11 ...
The renin receptor binds renin and prorenin. Binding of renin to this receptor induces the conversion of angiotensinogen to ... "Pivotal role of the renin/prorenin receptor in angiotensin II production and cellular responses to renin". J. Clin. Invest. 109 ... The renin receptor also known as ATPase H(+)-transporting lysosomal accessory protein 2, or the prorenin receptor, is a protein ... 2006). "Renin increases mesangial cell transforming growth factor-beta1 and matrix proteins through receptor-mediated, ...
Renin (Persian: رنين) may refer to: Renin-e Bozorg Renin-e Kuchek This disambiguation page lists articles about distinct ...
Direct renin inhibitors can also be used for hypertension. The drugs that inhibit renin are aliskiren and the investigational ... The renin-angiotensin system (RAS), or renin-angiotensin-aldosterone system (RAAS), is a hormone system that regulates blood ... PMID 9570034.[permanent dead link] Nguyen, G (March 2011). "Renin, (pro)renin and receptor: an update". Clinical Science. 120 ( ... into renin and secrete it directly into the circulation. Plasma renin then carries out the conversion of angiotensinogen, ...
... (Persian: رنين بزرگ, also Romanized as Renīn-e Bozorg; also known as Renīn-e Shams od Dīn) is a village in ... Renin-e Bozorg can be found at GEOnet Names Server, at this link, by opening the Advanced Search box, entering "10406724" in ...
... can be found at GEOnet Names Server, at this link, by opening the Advanced Search box, entering "10406724" in ... Renin-e Kuchek (Persian: رنين كوچك, also Romanized as Renīn-e Kūcheḵ) is a village in Gowharan Rural District, Gowharan ...
... (PRA), also known as the renin (active) assay or random plasma renin, is a measure of the activity of the ... Renin Direct. New Assays for Aldosterone, Renin and Parathyroid Hormone Archived 2011-10-27 at the Wayback Machine University ... Cloning and sequence analysis of cDNA for human renin precursor. PubMed. Pivotal role of the renin/prorenin receptor in ... Different secretory pathways of renin from mouse cells transfected with the human renin gene. 1988 Mar 5; PubMed Free text. ...
... (ARR) is the mass concentration of aldosterone divided by the plasma renin activity or by serum ... The aldosterone/renin ratio is recommended as screening tool for primary hyperaldosteronism. There is more than one way to ... 1] Aldosterone-Renin Ratio in Primary Hyperaldosteronism by Allan S. Brett. Posted: 03/15/2005; Journal Watch. 2005;4(2) (All ... If the inverse ratio (i.e. renin-to-aldosterone) ratio is used, a value lower than the cutoff indicates primary ...
... of the renin (REN) gene. It acts to regulate the levels of renin protein produced in the cell. Renin is secreted by renal ... untranslated region of human renin mRNA and differentially modulate renin expression". J. Biol. Chem. 278 (45): 44894-44903. ... Page for Renin stability regulatory element (REN-SRE) at Rfam v t e (Cis-regulatory RNA elements, All stub articles, Molecular ... The Renin stability regulatory element (REN-SRE) is a cis-acting element identified in the 3'untranslated region (3'UTR) ...
... is a peer-reviewed academic journal that publishes papers in the field of ... Journal of the Renin-Angiotensin-Aldosterone System is abstracted and indexed in, among other databases: SCOPUS, and the Social ... Journal of the Renin-Angiotensin-Aldosterone System is a resource for biomedical professionals, including basic scientists and ... Journal of the Renin-Angiotensin-Aldosterone System also publishes research on other peptides, such as vasopressin, the ...
Renin-e Bozorg , Renin-e Kuchek , Reza Alichi , Rezayi , Rezvan , Rig Deraz , Rig Kag , Rig Muled , Rig , Rig , Rigu , Riku , ...
Albert, Renin Wilben. "IPL 2021: [Watch] KKR players have a ball while enjoying a game of 'Maram Pitti'". www.sportskeeda.com. ...
... 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 ...
Rather, both renin and aldosterone are measured, and a resultant aldosterone-to-renin ratio (ARR) is used for case detection. A ... Tiu SC, Choi CH, Shek CC, Ng YW, Chan FK, Ng CM, Kong AP (January 2005). "The use of aldosterone-renin ratio as a diagnostic ... "Renin/Aldosterone Protocol". United Bristol Healthcare NHS Trust. Archived from the original on 2007-08-13. Funder JW, Carey RM ... The increased blood pressure will lead to increased glomerular filtration rate and cause a decrease in renin released from the ...
Therefore, the granular (JG) cells seem to be the only source of active renin. "Renin , Definition of Renin by Lexico". Lexico ... Prorenin (/prəˈriːnɪn/) is a protein that constitutes a precursor for renin, the hormone that activates the renin-angiotensin ... Morganti, Alberto (2019). "Renin and Prorenin". Encyclopedia of Endocrine Diseases. pp. 478-482. doi:10.1016/B978-0-12-801238- ... Blood concentration levels of prorenin are between 5 and 10 times higher than those of renin. There is evidence to suggest that ...
Renin activates a circulating liver derived prohormone angiotensinogen by proteolytic cleavage of all but its first ten amino ... The renin-angiotensin-aldosterone system is a major blood pressure regulating mechanism. Markers of electrolyte and water ... Renin and Angiotensin". In Brunton, Laurence L.; Lazo, John S.; Parker, Keith (eds.). Goodman & Gilman's The Pharmacological ... Luno J, Praga M, de Vinuesa SG (2005). "The reno-protective effect of the dual blockade of the renin angiotensin system (RAS ...
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 ...
At the same time, the juxtaglomerular cells sense the decrease in blood pressure and release renin. Renin converts ... Renin-angiotensin system (RAS): This system is generally known for its long-term adjustment of arterial pressure. This system ... Aldosterone release: This steroid hormone is released from the adrenal cortex in response to activation of the renin- ... Archived version 2009-10-03 Fountain, John; Lappin, SL (January 2022). Physiology, Renin Angiotensin System. Treasure Island, ...
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. ...
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. ... Farmakologija renin-angiotenzin sistema. Banja Luka, Medicinski fakultet, 2014. Igić R, Erdos EG, Yeh HS, Sorells K, Nakajima T ... Igić R, Škrbić R. The renin-angiotensin system and its blockers. Srp Arh Celok Lek 2014;142:756-63. Sokolova-Djokic L, Zizic- ...
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 ...
"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), ...
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 ...
Ruilope LM, Tamargo J (April 2017). "Renin-angiotensin system blockade: Finerenone". Nephrologie & Therapeutique. 13 Suppl 1: ...
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 ...
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 ...
Is COVID-19 Activating the Renin-Angiotensin System? In an editorial accompanying the European Heart Journal publication, Gavin ... Leading experts suggest that effects of the virus on the renin-angiotensin system may be the key to understanding why men and ... "As we believe the renin-angiotensin system is being over-activated by the virus, this could also explain why patients with ... Two new studies have been published that further focus attention on how the renin-angiotensin system - and specifically the ...
The effect of renin-angiotensin-aldosterone system inhibition with dual blockade, ACEI and angiotensin receptor antagonists, on ... Renal Volume, Renin-Angiotensin-Aldosterone System, Hypertension, and Left Ventricular Hypertrophy in Patients with Autosomal ... Renal Volume, Renin-Angiotensin-Aldosterone System, Hypertension, and Left Ventricular Hypertrophy in Patients with Autosomal ... Renal Volume, Renin-Angiotensin-Aldosterone System, Hypertension, and Left Ventricular Hypertrophy in Patients with Autosomal ...
Map of county-level variation in renin-angiotensin system antagonist (RASA) non-adherence among New York State Medicare Part D ... Map Details - County-level Variation in Renin-Angiotensin System Antagonist (RASA) Nonadherence Among New York. ...
We previously reported that Olfr78 plays a role in renin secretion in iso … ... Olfactory receptor 78 modulates renin but not baseline blood pressure Physiol Rep. 2021 Sep;9(18):e15017. doi: 10.14814/ ... In sum, these experiments suggest that Olfr78 modulates renin, but does not play an active role in blood pressure regulation at ... We previously reported that Olfr78 plays a role in renin secretion in isolated glomeruli, and that Olfr78 knockout (KO) mice ...
Renin. A, B. 340. Homo sapiens. Mutation(s): 0 Gene Names: REN, renin. EC: 3.4.23.15. ... Discovery of VTP-27999, an Alkyl Amine Renin Inhibitor with Potential for Clinical Utility.. Jia, L., Simpson, R.D., Yuan, J., ... Structure guided optimization of a series of nonpeptidic alkyl amine renin inhibitors allowed the rational incorporation of ... Structure guided optimization of a series of nonpeptidic alkyl amine renin inhibitors allowed the rational incorporation of ...
Recombinant Human Renin protein (denatured) is an Escherichia coli Full length protein 67 to 406 aa range, , 80% purity and ... Renin is a highly specific endopeptidase, whose only known function is to generate angiotensin I from angiotensinogen in the ...
Male dogs were catheterized to measure hepatic renal flow and plasma renin activity. The effects of lead, 0.5 milligrams per ... on the relationship between plasma renin and angiotensin II were studied. ... In some animals the effect of lead on the hepatic removal of renin was monitored by sampling hepatic portal blood. Plasma renin ... Hepatic removal of renin was shut off after 2 to 3 hours of lead administration. The authors conclude that the major cause of ...
... *Download PDF ... An umbrella review and meta-analysis of the use of renin-angiotensin system drugs and COVID-19 outcomes: what do we know so far ... Study: An umbrella review and meta-analysis of the use of renin-angiotensin system drugs and COVID-19 outcomes: what do we know ... Umbrella analysis of the effect of renin-angiotensin-aldosterone system inhibitors on COVID-19 related outcomes. News-Medical ...
Evaluated renin-angiotensin-aldosterone system (RAAS) inhibitor drugs and their maximum doses, listed in descending order of ... Evaluation of the Treatment Gap Between Clinical Guidelines and the Utilization of Renin-Angiotensin. , Volume 21. , Issue 11 ... eAPPENDIX 2. RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM INHIBITOR DRUGS AND MAXIMUM DOSE LEVELS. ...
Inactive Renin in Rabbit Plasma: Effect of Haemorrhage H. K. Richards; H. K. Richards ... H. K. Richards, S. A. Grace, A. R. Noble, K. A. Munday; Inactive Renin in Rabbit Plasma: Effect of Haemorrhage. Clin Sci (Lond) ... 1. Renin activity in rabbit plasma increases after acidification (pH 3·3), probably due to activation of an inactive form of ... 2. Both active and inactive renin in plasma increase after haemorrhage. This stimulus does not change the relative proportions ...
Phenytoin stimulates renin secretion from rat kidney slices.. P C Churchill, F D McDonald and M C Churchill ... Phenytoin stimulates renin secretion from rat kidney slices.. P C Churchill, F D McDonald and M C Churchill ... Phenytoin stimulates renin secretion from rat kidney slices.. P C Churchill, F D McDonald and M C Churchill ... Phenytoin stimulates renin secretion from rat kidney slices. Message Subject (Your Name) has forwarded a page to you from ...
Sodium butyrate suppresses angiotensin II-induced hypertension by inhibition of renal (pro)renin receptor and intrarenal renin- ... The intrarenal renin-angiotensin system: from physiology to the pathobiology of hypertension and kidney disease. Pharmacol Rev ... Olfactory receptor responding to gut microbiota-derived signals plays a role in renin secretion and blood pressure regulation. ... renin receptor (PRR) and renin, and therefore provide an improvement for Ang II-induced renal injuries[65]. Nevertheless, ...
As previously stated, renin and Ang II are two key members of the RAS (23). Therefore, the mRNA expression of renin and Ang II ... Calcitriol suppresses renin and Ang II expression in LPS-treated rat PMVECs. Increased renin activity stimulates the conversion ... Renin activity and angiotensin II assays. Renin activity and angiotensin II concentration in the bronchoalveolar lavage fluid ... is a negative endocrine regulator of the RAS and inhibits renin biosynthesis (16,27). Inhibition of the (pro)renin receptor ...
This study covers the latent demand outlook for renin-angiotensin system-blocking cardiovascular drugs across the states and ... The 2023-2028 Outlook for Renin-Angiotensin System-Blocking Cardiovascular Drugs in the United States. October 2022 , 515 pages ... This study covers the latent demand outlook for renin-angiotensin system-blocking cardiovascular drugs across the states and ... In this report we define the sales of renin-angiotensin system-blocking cardiovascular drugs as including all commonly ...
... ... Saravi B, Vollmer A, Lang G, Adolphs N, Li Z, Giers V, Stoll P. Impact of renin-angiotensin system inhibitors and beta-blockers ... The tissue renin-angiotensin system as new therapeutic target for treatment of disc degeneration ... Recently, our group identified the expression of a tissue Renin-Angiotensin System (tRAS) in human intervertebral discs (IVD). ...
CT+TT) of rs1894111 polymorphism in the ADRBK1 gene might be associated with low-renin hypertension in Han Chinese. ... Hypertensive patients were classified into 4 renin categories via PRA quartile. Single-nucleotide polymorphisms (SNPs) of the ... case-control study was designed to investigate the potential relationship between polymorphisms of ADRBK1 and plasma renin ... Renin is the first step of the RAS cascade, which is a major regulator of salt-volume homeostasis. Adrenergic beta receptor ...
Dual Renin-Angiotensin System Blockade in Heart Failure Academic Article * Dual inhibition of the renin-angiotensin system in ... Blocking the renin-angiotensin system: dual- versus mono-therapy Academic Article * Blood pressure-dependent and independent ... Renin-angiotensin and endothelial nitric oxide synthase gene polymorphisms are not associated with the risk of incident type 2 ... Stopping Renin-Angiotensin System Inhibitors in Patients with Advanced CKD and Risk of Adverse Outcomes: A Nationwide Study ...
The genomic DNAs that specify the renin mRNAs found in the submaxillary gland and in the kidney of Swiss mice have been ... To correlate the differential expression of the renin genes with their structures, a sequence analysis of the putative 5′ ... Mouse kidney and submaxillary gland renin genes differ in their 5′ putative regulatory sequences. ... Restriction maps of both renin genes and their flanking sequences are presented. ...
Renin 1 antibody LS-C331567 is an unconjugated rabbit polyclonal antibody to Renin 1 (REN) from human. It is reactive with ... Polyclonal Rabbit anti‑Human REN / Renin 1 Antibody (WB) LS‑C331567 Polyclonal Rabbit anti‑Human REN / Renin 1 Antibody (WB) LS ... Renin 1 antibody LS-C331567 is an unconjugated rabbit polyclonal antibody to Renin 1 (REN) from human. It is reactive with ...
Neural control of renin expression by microRNA in hypertension. *Head, Geoffrey A. (Primary Chief Investigator (PCI)) ...
... contain renin granules and release renin as evidenced by RT-PCR, immunocytochemistry and measurement of renin activity, ... contain renin granules and release renin as evidenced by RT-PCR, immunocytochemistry and measurement of renin activity, ... contain renin granules and release renin as evidenced by RT-PCR, immunocytochemistry and measurement of renin activity, ... contain renin granules and release renin as evidenced by RT-PCR, immunocytochemistry and measurement of renin activity, ...
The renin-angiotensin system (RAS) plays a critical role in the development of diabetic nephropathy, and blockade of the RAS is ... N2 - The renin-angiotensin system (RAS) plays a critical role in the development of diabetic nephropathy, and blockade of the ... AB - The renin-angiotensin system (RAS) plays a critical role in the development of diabetic nephropathy, and blockade of the ... abstract = "The renin-angiotensin system (RAS) plays a critical role in the development of diabetic nephropathy, and blockade ...
Albuminuria, Aliskiren, Diabetic nephropathy, Renin inhibition, Renin-angiotensin-system, Type 2 diabetes ... Inhibition of renin with an active site inhibitor, aliskiren, lowers blood pressure (BP) in diabetic patients. Here, we studied ... Time course of the antiproteinuric and antihypertensive effects of direct renin inhibition in type 2 diabetes. Publication. ... Time course of the antiproteinuric and antihypertensive effects of direct renin inhibition in type 2 diabetes. Kidney ...
3. The reflex control of renin release on postural change has been established. 4. The effect of diuretics on renin release has ... 3. The reflex control of renin release on postural change has been established. 4. The effect of diuretics on renin release has ... 3. The reflex control of renin release on postural change has been established. 4. The effect of diuretics on renin release has ... 3. The reflex control of renin release on postural change has been established. 4. The effect of diuretics on renin release has ...
... low MW alkylamine renin inhibitors. Oral adminstration of lead ... low MW alkylamine renin inhibitors. Oral adminstration of lead ...
Involvement of Renin-Angiotensin System in Pressure-Flow Relationship: Role of Angiotensin-converting Enzyme Gene Polymorphism ... Effects of Propranolol on the Cardiovascular and Renin-Angiotensin Systems during Hypotension Produced by Sodium Nitroprusside ... Terlipressin versus Norepinephrine to Counteract Anesthesia-induced Hypotension in Patients Treated with Renin-Angiotensin ... Effects of Propranolol on the Cardiovascular and Renin-Angiotensin Systems during Hypotension Produced by Sodium Nitroprusside ...
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1. Rice N, Freeman J, Porter L, Wright S, Rowland N. Single nucleotide polymorphisms of the renin angiotensin system linked to ... Rice N, Freeman J, Porter L, Wright S, Rowland N. Single nucleotide polymorphisms of the renin angiotensin system linked to ... Rice N and others, Single Nucleotide Polymorphisms of the Renin Angiotensin System Linked to High Prevalence of Essential ... Rice, N, et al.. "Single nucleotide polymorphisms of the renin angiotensin system linked to high prevalence of essential ...
Baral, R., Tsampasian, V., Debski, M., Moran, B., Garg, P., Clark, A., & Vassiliou, V. S. (2021). Association between renin- ... Baral, R, Tsampasian, V, Debski, M, Moran, B, Garg, P, Clark, A & Vassiliou, VS 2021, Association between renin-angiotensin- ... T1 - Association between renin-angiotensin-aldosterone system inhibitors and clinical outcomes in patients with COVID-19: A ... title = "Association between renin-angiotensin-aldosterone system inhibitors and clinical outcomes in patients with COVID-19: A ...
  • Structure guided optimization of a series of nonpeptidic alkyl amine renin inhibitors allowed the rational incorporation of additional polar functionality. (rcsb.org)
  • In a recent study posted to the medRxiv * preprint server, researchers conducted an umbrella review and meta-analysis of the renin-angiotensin-aldosterone system (RAAS) inhibitors' impact on coronavirus disease 2019 (COVID-19) clinical outcomes. (news-medical.net)
  • Data was gathered from medRxiv, the Cochrane Library, Scopus, Embase, and Medline (OVID) databases using keywords such as COVID-19, renin-angiotensin system, angiotensin II receptor antagonists, and angiotensin-converting enzyme inhibitors from the inception of the study until February 1, 2021. (news-medical.net)
  • Saravi B, Vollmer A, Lang G, Adolphs N, Li Z, Giers V, Stoll P. Impact of renin-angiotensin system inhibitors and beta-blockers on dental implant stability. (aofoundation.org)
  • One major problem for the current RAS inhibitors is the compensatory renin increase, which reduces the efficacy of RAS inhibition. (elsevier.com)
  • Angiotensin converting enzyme (ACE) inhibitors have the potential to falsely elevate plasma renin activity (PRA). (marshfieldlabs.org)
  • They also used since the forms of renin inhibitors in the body, the following variety of the kidneys, it may not help to lower blood pressure. (jewishledger.com)
  • Irbesartan: Increased risk of renin inhibitors, rapid kidney failure, and nerve impairment. (labelpack.lat)
  • Background and objectives Renin-angiotensin system (RAS) inhibitors reduce cardiovascular morbidity and mortality in patients with CKD. (elsevier.com)
  • Some blood pressure medications are considered safe to use during pregnancy , but angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor blockers and renin inhibitors are generally avoided during pregnancy . (psichologyanswers.com)
  • Renal Volume, Renin-Angiotensin-Aldosterone System, Hyperten. (lww.com)
  • Renal cyst enlargement in ADPKD in adults is associated with stimulation of both the circulating and intrarenal renin-angiotensin-aldosterone system. (lww.com)
  • The effect of renin-angiotensin-aldosterone system inhibition with dual blockade, ACEI and angiotensin receptor antagonists, on renal volume and kidney function is under study in the Halt Progression of Polycystic Kidney Disease (HALT PKD) trial. (lww.com)
  • Male dogs were catheterized to measure hepatic renal flow and plasma renin activity. (cdc.gov)
  • 3. After ligation of the renal blood vessels neither form of renin increases in response to haemorrhage. (portlandpress.com)
  • Here we demonstrated that combination therapy with an AT1 receptor blocker and a vitamin D analog markedly ameliorated renal injury in the streptozotocin (STZ)-induced diabetes model due to the blockade of the compensatory renin rise by the vitamin D analog, leading to more effective RAS inhibition. (elsevier.com)
  • The renal juxtaglomerular apparatus generates renin, an enzyme that converts angiotensinogen to angiotensin I. The inactive angiotensin I is enzymatically converted to the active octapeptide angiotensin II, a potent vasopressor responsible for hypertension of renal origin. (marshfieldlabs.org)
  • Renin secretion by the kidney is stimulated by a fall in glomerular blood pressure, by decreased sodium concentration at the macula densa at the distal tubule, or by stimulation of sympathetic outflow to the kidney, such as in renal vascular diseases. (marshfieldlabs.org)
  • Kidney disease, such as unilateral renal artery stenosis, results in elevated renin and aldosterone levels. (marshfieldlabs.org)
  • as well as the renin how to control hereditary high blood pressure is associated with a basic valve that renal rate is not important to promote the pills. (jewishledger.com)
  • Endopeptidasa muy específica (Leu-Leu) que forma ANGIOTENSINA I a partir de su precursor, el ANGIOTENSINÓGENO, desencadenando una cascada de reacciones que elevan la PRESIÓN ARTERIAL y aumentan la retención renal de sodio en el SISTEMA RENINA-ANGIOTENSINA. (bvsalud.org)
  • Cyclooxygenase enzymes, which regulate the conversion of arachidonic acid to prostaglandins, are abundantly present in the kidneys and play an important role in renal hemostasis, renin release, renal tubular salt and water reabsorption. (sportsmedreview.com)
  • Renin is a highly specific endopeptidase, whose only known function is to generate angiotensin I from angiotensinogen in the plasma, initiating a cascade of reactions that produce an elevation of blood pressure and increased sodium retention by the kidney. (abcam.com)
  • 5. In the rabbit, therefore, the kidney is a major source of the inactive renin in plasma. (portlandpress.com)
  • Phenytoin stimulates renin secretion from rat kidney slices. (aspetjournals.org)
  • The genomic DNAs that specify the renin mRNAs found in the submaxillary gland and in the kidney of Swiss mice have been isolated by molecular cloning in phage lambda. (pasteur.fr)
  • The aim of the present study was dual: first to establish that a preparation of afferent arterioles freshly isolated from the rat kidney is a suitable model to study renin release and synthesis, and second to investigate the effect(s) of nitric oxide (NO) inhibition on renin release in this model. (elsevier.com)
  • 2. Experimental evidence has been obtained that sympathetic stimulation releases renin from the kidney independently of local vasomotor changes. (elsevier.com)
  • Renin-1 is also known as Ren, Angiotensinogenase or Kidney rennin. (bosterbio.com)
  • Renin is secreted from juxtaglomerular kidney cells. (reninsignaling.com)
  • Background: Renin-angiotensin system blockers (RASBs) reduce end-stage kidney disease and cardiovascular event (CVE) development in chronic kidney disease. (elsevier.com)
  • the Japan Academic Consortium of Kidney Transplantation (JACK) Investigators 2020, ' Effect of renin-angiotensin system blockade on graft survival and cardiovascular disease in kidney transplant recipients: retrospective multicenter study in Japan ', Clinical and Experimental Nephrology , vol. 24, no. 4, pp. 369-378. (elsevier.com)
  • A high renin value can mean that kidney disease, blockage of an artery leading to a kidney, Addison's disease , cirrhosis , excessive bleeding (hemorrhage), or a hypertensive emergency is present. (bvobgyn.com)
  • A low renin value can mean that some types of kidney disease or Conn's syndrome is present. (bvobgyn.com)
  • 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. (bvsalud.org)
  • This is due possibly to the follicles functioning as faulty glomerulii (the glomerulus is the filtering apparatus of the kidney and usually retains sodium and potassium) as well as the alterations in the renin-angiotensin system which I alluded to above. (plan-b-chronicles.com)
  • We previously reported that Olfr78 plays a role in renin secretion in isolated glomeruli, and that Olfr78 knockout (KO) mice have lower plasma renin activity. (nih.gov)
  • Renin secretion was increased in isolated afferent arterioles after in vivo treatment with the diuretic furosemide (+300%) or in vitro treatment with the adenylyl cyclase activator forskolin (+50%), indicating that this vascular preparation responds appropriately to regulators of the reninangiotensin system. (elsevier.com)
  • This study was designed to determine the effects of synthetic rat atrial natriuretic factor (ANF) on plasma renin activity (PRA) and aldosterone secretion in separate groups of normal and potassium-loaded anesthetized rats. (elsevier.com)
  • These results indicate that ANF can inhibit chronic potassium-stimulated aldosterone secretion in the rat independently of its inhibitory actions on renin release. (elsevier.com)
  • Inhibition of ACE results in decreased plasma angiotensin II and increased plasma renin activity (PRA), the latter resulting from loss of negative feedback on rennin release caused by reduction in angiotensin II.The reduction of angiotensin II leads to decreased aldosterone secretion, and, as a result, small increases in serum potassium may occur along with sodium and fluid loss. (nih.gov)
  • To verify that the lack of regulation of renin release after L-NAME treatment was due to NO inhibition, the NO donor 3-morpholino-syndonimin-hydrochloride (SIN-1) was administered in afferent arterioles or cortical slices from kidneys of L-NAME-treated rats. (elsevier.com)
  • Inhibition of renin with an active site inhibitor, aliskiren, lowers blood pressure (BP) in diabetic patients. (eur.nl)
  • Here, we studied the time course of the antihypertensive and antiproteinuric effect of renin inhibition in 15 patients with type 2 diabetes and elevated urinary albumin/creatinine ratios (UACRs) to check whether aliskiren can decrease proteinuria. (eur.nl)
  • Brands, MW & Freeman, RH 1989, ' Aldosterone and renin inhibition by atrial natriuretic factor in potassium-loaded rats ', American Journal of Physiology - Regulatory Integrative and Comparative Physiology , vol. 257, no. 6, pp. 26/6. (elsevier.com)
  • Freeman, R. H. / Aldosterone and renin inhibition by atrial natriuretic factor in potassium-loaded rats . (elsevier.com)
  • It is nature's own inhibitor of the renin-angiotensin system, breaking down harmful angiotensin II to the protective angiotensin 1-7," he said. (medscape.com)
  • As we believe the renin-angiotensin system is being over-activated by the virus, this could also explain why patients with underlying cardiovascular diseases are having worse outcomes and would suggest that taking an ACE inhibitor or ARB would actually be protective. (medscape.com)
  • In afferent arterioles isolated from rats chronically treated with the NO-synthase inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME), forskolin was ineffective in modifying renin release despite stimulation of cAMP levels. (elsevier.com)
  • Renin Angiotensin Aldosterone System Blockade: Little to No Rationale for ACE Inhibitor and ARB Combinations. (medbullets.com)
  • Comparative Effects of Direct Renin Inhibitor and Angiotensin Receptor Blocker on Albuminuria in Hypertensive Patients with Type 2 Diabetes. (bvsalud.org)
  • We compared the effect of aliskiren, a direct renin inhibitor (DRI), with that of angiotensin receptor blockers (ARBs) on albuminuria and urinary excretion of angiotensinogen , a marker of intrarenal renin-angiotensin system activity. (bvsalud.org)
  • Renin-angiotensin system inhibitor exerts prognostic effects in HFpEF patients with low baseline chloride level. (twmu.ac.jp)
  • The present case-control study was designed to investigate the potential relationship between polymorphisms of ADRBK1 and plasma renin activity (PRA) in hypertension. (medscimonit.com)
  • The dominant model (CC vs. CT+TT) of rs1894111 polymorphism in the ADRBK1 gene might be associated with low-renin hypertension in Han Chinese. (medscimonit.com)
  • INTRODUCTION: Recent animal studies have shown that the alternate renin-angiotensin system (RAS) consisting of angiotensin-converting enzyme 2 (ACE2), angiotensin-(1⁻7) (Ang-(1⁻7)) and the Mas receptor is upregulated in cirrhosis and contributes to splanchnic vasodilatation and portal hypertension. (sdu.dk)
  • A renin assay blood test is done to find the cause of high blood pressure (hypertension) . (bvobgyn.com)
  • A renin test is done to find the cause of high blood pressure (hypertension), especially when potassium levels in the blood are low. (bvobgyn.com)
  • The renin-angiotensin system (RAS) is an important regulator of cirrhosis and portal hypertension. (elsevier.com)
  • Its beneficial effects in hypertension and heart failure appear to result primarily from suppression of the renin-angiotensin-aldosterone system. (nih.gov)
  • Lead, hypertension, and the renin-angiotensin system in rats. (cdc.gov)
  • They are the most common side effects or occurred to be more effective, such as caffeine, and other drugs are also prescribed for drugs to treat high blood pressure hypertension drugs for renin-angiotensin cascade . (kedirikota.go.id)
  • Does Renin-Angiotensin System Blockade Protect Lupus Nephritis Patients From Atherosclerotic Cardiovascular Events? (mcmaster.ca)
  • The renin-angiotensin system (RAS) plays a critical role in the development of diabetic nephropathy, and blockade of the RAS is currently used for treatment of diabetic nephropathy. (elsevier.com)
  • These were accompanied by blockade of intrarenal renin and Ang II accumulation induced by hyperglycemia and losartan. (elsevier.com)
  • Combining these classes, for the purpose of enhancing renin-angiotensin-aldosterone system blockade and incremental blood pressure, nephroprotective, and cardioprotective effects, logically has emerged as an area for scientific inquiry and clinical use. (medbullets.com)
  • CONCLUSIONS: The low plasma renin concentrations, even under RAAS blockade, in CD may be the consequence of increased GC-mediated MR stimulation and/or the elevated angiotensinogen levels in such patients. (ru.nl)
  • Renin is a hormone made by the kidneys. (medlineplus.gov)
  • Renin is an enzyme made by special cells in the kidneys . (bvobgyn.com)
  • Renin, an enzyme synthesized by the kidneys, is released into the circulation where it acts on a plasma globulin substrate to produce angiotensin I, a relatively inactive decapeptide. (nih.gov)
  • The ACE converts angiotensin decapeptide inactive form into active octapeptide angiotensin II in the kidneys, especially in the renin-angiotensin-aldosterone system 13 . (ijpsr.com)
  • Glucocorticoids (GC) modulate the renin-angiotensin-aldosterone system (RAAS) among others by increasing hepatic angiotensinogen expression and stimulating mineralocorticoid receptors (MR). This study therefore evaluated plasma RAAS components in CD patients before and after drug therapy. (ru.nl)
  • RESULTS: Baseline concentrations of angiotensinogen were elevated, while renin and aldosterone were low and suppressed, respectively, even in patients treated with RAAS-blockers. (ru.nl)
  • Therapeutisch werden standardmäßig Medikamente zur Senkung des Blutzuckerspiegels (Inhibitoren des Renin-Angiotensin-Aldosteron-Systems (RAAS), Metformin, Inhibitoren des Natrium-Glucose-Transporters-2 (SGLT2) und des Blutdrucks (Erstlinien Therapie mit Inhibitoren des RAAS, sekundäre Therapie mit Statinen sowie Nikotinentwöhnung und salzarme Ernährung) eingesetzt. (uni-muenchen.de)
  • The body's renin-angiotensin-aldosterone system (RAAS) includes hormones that affect blood pressure regulation, and dysregulation of the RAAS can lead to the development of high blood pressure. (ladyinrainbow.com)
  • The renin-angiotensin (Ang) system (RAS), which includes Ang I-converting enzyme (ACE) and ACE2, is a complex network that has a major role in various biological functions, including blood pressure regulation and water balance. (spandidos-publications.com)
  • Neural control of renin release. (elsevier.com)
  • 1. Factors involved in the neural control of renin release have been reviewed. (elsevier.com)
  • 3. The reflex control of renin release on postural change has been established. (elsevier.com)
  • 6. The pathological significance of the neural control of renin release has been discussed. (elsevier.com)
  • Dive into the research topics of 'Neural control of renin release. (elsevier.com)
  • In addition, the correlation between renin release and tissue renin content was disrupted. (elsevier.com)
  • However, there is no consistent correlation between renin levels and response to the drug. (nih.gov)
  • To investigate the relation between renin content in each juxtaglomerular apparatus and reduction of plasma renin activity (PRA) with aging, the PRA and microdissected superficial or juxtamedullary single nephron renin content (SNRC) were determined in 5 young (3-6 mth) and 5 aged (13-18 mth) rats fed on a normal salt diet. (elsevier.com)
  • It is suggested that decreased synthesis of renin in each juxtaglomerular apparatus is an important factor in the decreased PRA observed with aging. (elsevier.com)
  • The effects of lead (7439921) on the relationship between plasma renin and angiotensin II were studied. (cdc.gov)
  • Plasma renin activity rose significantly over the 3 hour period of lead exposure. (cdc.gov)
  • Although there was a linear relationship between angiotensin II levels and plasma renin activity following nonlead stimuli, this relation was changed with lead lowered angiotensin II levels. (cdc.gov)
  • The authors conclude that the major cause of increased plasma renin activity after lead administration is the cessation of hepatic removal of renin and lead prevents angiotensin II levels from rising proportionately with plasma renin activity. (cdc.gov)
  • IMSEAR at SEARO: Plasma renin activity in normotensive Indian population. (who.int)
  • Patient Preparation: The plasma renin activity cannot be interpreted if the patient is being treated with spironolactone (Aldactone). (marshfieldlabs.org)
  • Stalker HP, Holland NH, Kotchen JM, Kotchen TA: Plasma renin activity in healthy children. (marshfieldlabs.org)
  • A high ratio of serum aldosterone (SA) in ng/dL to plasma renin activity (PRA) in ng/mL per hour, is a positive screening test result, a finding that warrants further testing. (marshfieldlabs.org)
  • Arterial blood samples were obtained to evaluate plasma renin activity (PRA) and norepinephrine (NE). (unthsc.edu)
  • The ACE genotype was assessed by amplification of the ACE gene polymorphism in the presence of RsaI (plasma renin activity) and NlaIII restriction sites, by using a polymerase chain reaction (PCR) method. (royalmarloiesport.com)
  • These microvessels express preprorenin mRNA, contain renin granules and release renin as evidenced by RT-PCR, immunocytochemistry and measurement of renin activity, respectively. (elsevier.com)
  • 2. Both active and inactive renin in plasma increase after haemorrhage. (portlandpress.com)
  • 4. One day after bilateral nephrectomy no inactive renin could be demonstrated in plasma. (portlandpress.com)
  • Angiotensinogen is converted to angiotensin I by renin. (cebm.net)
  • The role of the sympathetic nervous system, epinephrine, norepinephrine, adrenocorticotrophic hormone, and the renin angiotensin aldosterone system in the control of blood pressure was discussed. (cdc.gov)
  • Results from reverse transcription‑quantitative polymerase chain reaction, western blotting and ELISA analysis demonstrated that calcitriol also modulated the expression of members of the renin‑angiotensin system (RAS), including angiotensin (Ang) I‑converting enzymes (ACE and ACE2), renin and Ang II, which indicates that calcitriol may exert protective effects on LPS‑induced lung injury, at least partially, by regulating the balance between the expression of members of the RAS. (spandidos-publications.com)
  • Mouse Renin 1/Ren1 ELISA Kit PicoKine™ (96 Tests). (bosterbio.com)
  • Furthermore, in afferent arterioles isolated from control rats, renin release was positively correlated with total renin content (r = 0.85). (elsevier.com)
  • Hypertensive patients were classified into 4 renin categories via PRA quartile. (medscimonit.com)
  • Single nucleotide polymorphisms of the renin angiotensin system linked to high prevalence of. (annalsofglobalhealth.org)
  • 4. The effect of diuretics on renin release has been studied and evidence of neural and non-neural mechanisms obtained. (elsevier.com)
  • Two new studies have been published that further focus attention on how the renin-angiotensin system - and specifically the ACE2 receptor - may be involved in COVID-19 infection. (medscape.com)
  • In comments to Medscape Medical News , Oudit, who has researched extensively on ACE2, put forward a hypothesis that the COVID-19 virus could be bringing about its harmful effects by causing an over-activation of the renin-angiotensin system. (medscape.com)
  • By activating ADAM-17 the virus causes shedding of ACE2 from tissue into plasma, and the reduction of ACE2 in tissue leads to over-activation of the renin-angiotensin system in tissues, which causes cardiovascular disease to get worse," Oudit explained. (medscape.com)
  • the findings suggest that renin release is in some way dependent on neural mechanisms. (elsevier.com)
  • Renin 1 antibody LS-C331567 is an unconjugated rabbit polyclonal antibody to Renin 1 (REN) from human. (lsbio.com)
  • 2017. Expression of renin-angiotensin system (RAS) components in endometrial cancer. (edu.au)
  • In some animals the effect of lead on the hepatic removal of renin was monitored by sampling hepatic portal blood. (cdc.gov)
  • Hepatic removal of renin was shut off after 2 to 3 hours of lead administration. (cdc.gov)
  • Because the two hormones work together, an aldosterone test is often done at the same time as a renin test. (medlineplus.gov)
  • 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)
  • In sum, these experiments suggest that Olfr78 modulates renin, but does not play an active role in blood pressure regulation at baseline, and is more likely activated by high levels of short chain fatty acids or hypotensive events. (nih.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. (bvobgyn.com)
  • An umbrella review and meta-analysis of the use of renin-angiotensin system drugs and COVID-19 outcomes: what do we know so far? (news-medical.net)
  • This study covers the latent demand outlook for renin-angiotensin system-blocking cardiovascular drugs across the states and cities of the United States. (marketpublishers.com)
  • Using econometric models which project fundamental economic dynamics within each state and city, latent demand estimates are created for renin-angiotensin system-blocking cardiovascular drugs. (marketpublishers.com)
  • In this report we define the sales of renin-angiotensin system-blocking cardiovascular drugs as including all commonly understood products and/or services falling within this broad category, irrespective of product packaging, formulation, size, or form. (marketpublishers.com)
  • Blood-Brain Barrier Crossing Renin-Angiotensin System Drugs: Considerations for Dementia and Cognitive Decline. (cornell.edu)
  • BACKGROUND/AIM: Renin-angiotensin system (RAS) is present in a diverse type of cells and plays an important role in lung physiology and pathophysiology. (bvsalud.org)
  • We have shown that vitamin D exerts renoprotective actions by transcriptionally suppressing renin. (elsevier.com)
  • Potential functional profiles of gut microbiome in amino acid metabolism, lipid biosynthesis proteins and steroid biosynthesis were remarkably increased, while the capacity in renin-angiotensin system was remarkably decreased following vaccines. (imrpress.com)
  • Recently, our group identified the expression of a tissue Renin-Angiotensin System (tRAS) in human intervertebral discs (IVD). (aofoundation.org)
  • To correlate the differential expression of the renin genes with their structures, a sequence analysis of the putative 5′ regulatory sequences of both genes was conducted. (pasteur.fr)
  • Similar results were obtained when cortical slices were used instead of afferent arterioles, suggesting that this defect in the regulation of renin release is independent of the presence of macula densa cells. (elsevier.com)
  • Restriction maps of both renin genes and their flanking sequences are presented. (pasteur.fr)
  • 1. Renin activity in rabbit plasma increases after acidification (pH 3·3), probably due to activation of an inactive form of renin. (portlandpress.com)
  • An increased renin-angiotensin system activity has been reported to play an important role in the pathological processes in these conditions. (bvsalud.org)
  • Hepcidin is potential regulator for renin activity. (cdc.gov)
  • Local authorities renin activity that there are so memorizing the for tracking periods we teenagers to have to end of although, in activity with leads to a third the drug local authority been the times. (hotelvikasinn.com)
  • If renin and/or aldosterone levels are not normal, it can be a sign of a serious adrenal gland disorder . (medlineplus.gov)
  • We also report that Olfr78KO mice have lower renin protein levels associated with glomeruli. (nih.gov)
  • In some people, it may be normal to have high blood levels of both renin and aldosterone. (bvobgyn.com)
  • If renin levels are low and aldosterone levels are high, a tumor may be present in the adrenal glands. (bvobgyn.com)
  • A simplified version of the pharmacology of the renin-angiotensin system is shown in the diagram below. (cebm.net)
  • A renin test (or renin and aldosterone test) is used to find out if the adrenal glands are making too much or too little aldosterone. (medlineplus.gov)