Optimized determination of angiotensin I-converting enzyme activity with hippuryl-l-histidyl-l-leucine as substrate

Schnaith, Ebbo; Beyrau, Ralf; Bückner, Brigitte; Klein, Rolf Michael; Rick, Wirnt

doi:10.1016/0009-8981(94)90143-0

Cited by 19 publications

(11 citation statements)

References 29 publications

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“…For evaluation of the effectiveness of treatment with ACE-I on serum ACE activity, two groups of patients were examined at the end of the follow-up in 2003 to 2005: A random group of 24 patients who had never been treated with ACE-I and a random group of 21 patients who had been treated with ACE-I for Ͼ4 yr. From both groups of patients, serum was obtained for measurements of serum ACE activity using a previously described method (18). In brief, this method is based on the determination of hippuric acid, generated in vitro during cleavage of synthetic substrate Hippuryl-His-Leu by ACE in serum, incubated under controlled condition.…”

Section: Methodsmentioning

confidence: 99%

“…In brief, this method is based on the determination of hippuric acid, generated in vitro during cleavage of synthetic substrate Hippuryl-His-Leu by ACE in serum, incubated under controlled condition. Concentration of hippuric acid is measured after extraction by a spectrophotometric method at 228 nm (18). ACE activity is expressed in international milliunits as nanomoles of hippuric acid generated during 1 min at 37°C per 1 ml of serum (mU/ml).…”

Section: Methodsmentioning

confidence: 99%

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Determinants of Progression from Microalbuminuria to Proteinuria in Patients Who Have Type 1 Diabetes and Are Treated with Angiotensin-Converting Enzyme Inhibitors

Ficociello¹,

Perkins²,

Silva³

et al. 2007

Clinical Journal of the American Society of Nephrology

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The aims of this study were to assess the frequency and determinants of (1) treatment with angiotensin-converting enzyme inhibitors (ACE-I) and (2) progression to proteinuria in the presence of ACE-I treatment in patients with type 1 diabetes and microalbuminuria. A clinic-based cohort study of patients with type 1 diabetes was begun in 1991. The patients who were included in this study (n ‫؍‬ 373) are the cohort members who received a diagnosis of microalbuminuria during a 2-yr baseline observation and were followed for 10 yr with frequent assessments of urinary albumin excretion and biennial examinations. Progression to proteinuria occurred when the median urinary albumin excretion during a 2-yr interval exceeded 299 g/min. During the decade-long study, the proportion of patients who had a history of microalbuminuria and were treated with ACE-I rose from 17 to 67%. Patients who started this treatment had (on average) higher BP, higher urinary albumin excretion, and longer diabetes duration than those who did not. Microalbuminuria often progressed to proteinuria (6.3/100 person-years) in those who were treated. Poor glycemic control and elevated serum cholesterol were the major determinants/predictors of this progression. Although treatment with ACE-I increased during the past decade, it was not completely effective, because microalbuminuria progressed to proteinuria in many treated patients. Poor glycemic control and elevated serum cholesterol were the major determinants/predictors for progression while on ACE-I treatment. The mechanisms that are responsible for the frequent failure of ACE-I to prevent progression of microalbuminuria to proteinuria in a clinical setting are not clear.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Determinants of Progression from Microalbuminuria to Proteinuria in Patients Who Have Type 1 Diabetes and Are Treated with Angiotensin-Converting Enzyme Inhibitors

Ficociello¹,

Perkins²,

Silva³

et al. 2007

Clinical Journal of the American Society of Nephrology

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“…Plasma (blood collected on 2.7 mM EDTA) was used for the measurement of glucose, cholesterol, and creatinine levels (using the Sigma kits). The activity of angiotensin-converting enzyme (ACE) was evaluated in serum as described by Schnaith et al (1994).…”

Section: Experimental Animalsmentioning

confidence: 99%

Beneficial effects of L -arginine supplementation in experimental hyperlipemia-hyperglycemia in the hamster

Popov¹,

Costache²,

Georgescu³

et al. 2002

Cell and Tissue Research

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The objective of this study was to evaluate whether administration of L-arginine, the substrate for nitric oxide synthesis, was able to ameliorate the endothelial dysfunction and the morphological changes induced by the combined insult of hyperlipemia and hyperglycemia. To this purpose, golden Syrian hamsters were rendered simultaneously hyperlipemic and diabetic (HD group) for 24 weeks, and then orally treated with 622.14 mg/kg per day L-arginine, for 12 weeks (HD + L-arg group). The following assays were carried out: (1) spectrophotometric: concentrations of circulating glucose, cholesterol, and creatinine, the activity of angiotensin-converting enzyme (ACE), and the osmotic fragility of erythrocyte plasmalemma; (2) myographic: the endothelium-dependent and -independent relaxation of the resistance arteries (i.d. 210-250 microm) to 10(-8) to 10(-4) M acetylcholine (ACh) or sodium nitroprusside (SNP); and (3) electron-microscopic: the ultrastructure of the resistance arteries, myocardium, and kidney glomeruli, which are main targets of hypertensive complications. The results showed that oral supplementation with L-arginine in simultaneous hyperlipemia-hyperglycemia induced in hamsters had favorable effects on: (1) homeostasis, i.e., diminished the concentration of circulating glucose (by ~63%) and cholesterol (by approximately 10%), reduced the ACE activity (by approximately 45%), and lowered the osmotic fragility of erythrocyte plasmalemma (as marker for the oxidative stress in plasma); (2) mesenteric resistance arteries, which showed (in 10(-4) M ACh) an improved endothelium-dependent relaxation (72.40+/-4.6% in the HD + L-arg group vs 61.90+/-1.45% in the HD group) and a reduced thickness (approximately 1.32-fold) of the smooth muscle cells' extracellular matrix; and (3) the heart, which displayed approximately 16% diminishing of the thickness of the left ventricular wall, and an apparently normal structure of the myocardium; the restoration of the thickness of the pericapillary extracellular matrix to almost normal dimensions was also observed. Administration of L-arginine did not modify the high level of plasma creatinine determined for the HD group (approximately 48% increased vs control group) and had no effect on the thickened, nodular basal lamina of the kidney capillaries. The results indicate that endothelial dysfunction established in combined hyperlipemia-diabetes is distinctive for each vascular bed (mesenteric arterioles, heart capillaries, kidney glomerular capillaries), and there is a reversible stage of the dysfunction in which L-arginine oral supplementation induced beneficial effects.

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“…[20] (b) The usage of 4-(2-hydroxyethyl)-1-piperazineethanesulfonic acid (HEPES) to stop the reaction and Cyanuric chloride in 1,4-dioxane as a color reagent measured in photometry at a wavelength of 504 nm. [29] (c) The addition of o-Phthaldialdehyde which then react with the substrate hydrolysis histidine-leucine is measured by a fluoro-colorimeter instrument at a wavelength of 495 nm emission and 365 nm excitation. [30] (d) The use of benzene-sulfonyl-chloride (BSC) as a color reagent in the presence of quinoline[31] (referred to as BSC-visible spectrophotometry method) and then modified using a microtiter plate reader.…”

Section: Resultsmentioning

confidence: 99%

Review of angiotensin-converting enzyme inhibitory assay: Rapid method in drug discovery of herbal plants

Ahmad¹,

Yanuar²,

Mulia³

et al. 2017

Phcog Rev

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The renin-angiotensin-aldosterone system is a signaling pathway which responsible in the blood pressure regulation. Angiotensin-converting enzyme (ACE) is one of the key elements responsible for the hypertensive mechanism. It converts angiotensin-I to angiotensin-II. The discovery history of the ACE inhibitory activity assay method has been through a long stage for decades and development continues until today. The ACE inhibitory activity has become an effective screening method in the search for new antihypertensive agents from herbal plants. Some of in vitro assay methods were used to examine the activity of ACE inhibitors based on the substrate usage, such as; Cushman and Cheung Method using a substrate hippuryl-histidyl-leucine (HHL), Holmquist method using a substrate furanacryloyl-tripeptide, Elbl and Wagner method using a substrate benzoil-[l-14C] glicyl-L-histidine-L-leucine, Carmel and Yaron method using a substrate o-aminobenzoylglycyl-p-nitrophenylalanilproline, and Lam method using 3-hydroxybutyrylglycyl-glycyl-glycine as substrate. Several different methods to measure the results of enzymatic reactions or separating substrate with products, including spectrophotometric, fluorometric, high-performance liquid chromatography, electrophoresis, and radiochemistry. Application of the test method for screening the ACE inhibitors activity and investigation of active compounds from natural products can be done easily with this method, it is very helpful in research because the results obtained are simple, accurate, and rapid.

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Optimized determination of angiotensin I-converting enzyme activity with hippuryl-l-histidyl-l-leucine as substrate

Cited by 19 publications

References 29 publications

Determinants of Progression from Microalbuminuria to Proteinuria in Patients Who Have Type 1 Diabetes and Are Treated with Angiotensin-Converting Enzyme Inhibitors

Determinants of Progression from Microalbuminuria to Proteinuria in Patients Who Have Type 1 Diabetes and Are Treated with Angiotensin-Converting Enzyme Inhibitors

Beneficial effects of L -arginine supplementation in experimental hyperlipemia-hyperglycemia in the hamster

Review of angiotensin-converting enzyme inhibitory assay: Rapid method in drug discovery of herbal plants

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