Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.4.15.1 (ACE)
18,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Antiontensin-converting enzyme (peptidyldipeptide hydrolase, EC 3.4.15.1) has been solubilized from canine pulmonary particles and purified to apparent homogeneity. A value of approx. 140000 was estimated for the molecular weight of the native and the reduced, denatured forms of the enzyme. No free NH2-terminal residue was detected by the dansylation procedure. Carbohydrate accounted for 17% of the weight of the enzyme, and the major residues were galactose, mannose and N-acetylglucosamine with smaller amounts of sialic acid and fucose. Removal of sialic acid residues with neuraminidase did not alter enzymatic activity. The enzyme contained one molar equivalent of zinc. Addition of this metal reversed stimulation and inhibition of activity observed in the presence of Co2+ and Mn2+, respectively. Immunologic homology of pure dog and rabbit enzymes was demonstrable with goat antisera. Fab fragments and intact IgG antibodies displayed similar inhibition dose vs. response curves with homologous enzyme, whereas the fragments were poor inhibitors of heterologous activity compared to the holoantibodies. The canine glycoprotein was much less active than the rabbit preparation in catalyzing hydrolysis of Hip-His-Leu. In contrast, the two enzymes exhibited comparable kinetic parameters with angiotensin I as substrate.
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PMID:Canine pulmonary angiotensin-converting enzyme. Physicochemical, catalytic and immunological properties. 20 22

Analysis of carcinoembryonic antigen (CE)-reactive glycoproteins from liver metastasis of primary colon and breast tumors and from primary breast tumors has been carried out by affinity chromatography on concanavalin A (Con A)-Sepharose. Three CEA-reactive glycoproteins from colon tumors (liver metastasis) with different binding capacity to Con A have been separated and further purified by gel filtration. Of the 3 CEA-reactive glycoproteins, 1 of them did not bind to Con A. Both Con A-binding and nonbinding CEA-reactive glycoproteins were immunologically indistinguishable when tested with a reference goat anti-CEA (ACE, 67-70; Dr. C.W. Todd and Dr. M.L. Egan), as well as with a variety of rabbit anti-CEA and anti-CEA (nonbinding) prepared in this laboratory. Carbohydrate analysis showed that mannose content of different purified CEA preparations or nonbinding CEA did not differ appreciably. N-Acetylglucosamine content of purified CEA preparations, however, varied considerably, suggesting that this sugar may impart the specificity of binding of CEA to Con A. The purified CEA preparations differed in their ability to inhibit the binding of 125l-labeled CEA to goat anti-CEA. One of the purified CEA preparations had 3- to 8-fold greater inhibitory capacity when compared to other preparations and shared a partial identity with a glycoprotein present in the extracts of fetal colon. The glycoprotein extracts of primary breast tumors did not contain a CEA that was immunologically identical to CEA present in colon tumors, whereas the liver metastasis of primary breast tumors showed several CEA-reactive glycoproteins as judged by radioimmunoassay. However, these CEA-reactive glycoproteins did not have any antigenic relationship with CEA from colon tumors when tested by double diffusion and immunoelectrophoresis. In conclusion, when Con A affinity chromatography of tumor glycoproteins is carried out under defined conditions and with the use of appropriate antisera, it is possible to delineate the presence or absence of CEA in tumors of nonentodermal origin.
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PMID:Immunochemical studies on carcinoembryonic antigen-reactive glycoproteins from carcinomas of the colon and breast separated by concanavalin A affinity chromatography. 97 8

We have investigated the effective role of angiotensin II on the renal function and urinary excretion of some prostanoids in healthy women submitted to different conditions of potassium balance. To this aim we have evaluated the effects of an acute inhibition of angiotensin converting enzyme by enalapril (E). The renal function was explored by clearance (cl.) method during induced hypotonic polyuria (oral water load followed by 5% dextrose solution infusion). During 60 min cl. period the urinary PGE2, 6-keto-PGF1 alpha and TxB2 were determined by RIA method. Each subject received paired studies, in absence and presence of E (10 mg administered per os 1 hour before the water load). Basal values of plasma renin activity (PRA) and urinary aldosterone (excreted during the 24 hours before the water load) were also determined by RIA method. This study protocol was applied in normal potassium balance (n = 6) and induced moderate potassium depletion (n = 6). This paper concerns the group in normal potassium balance in both absence (N3) and presence of E (N3.E). All subjects were submitted to normal dietary intake of sodium (150 mmol/d) and potassium (50 mmol/d). The basal values of PRA, urinary aldosterone and plasma electrolytes were in the normal range. The only significant effect produced by E was a reduction in mean arterial pressure, without significant changes in creatinine cl., urinary hydro-electrolyte excretions as well as urinary excretions of prostanoids.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Renal effects of the acute inhibition of angiotensin-converting enzyme. I. 1) Studies during normal sodium and potassium balance]. 129 5

We have investigated the relative roles of angiotensin II on the renal function and urinary excretion of some prostanoids in healthy women submitted to different conditions of potassium balance. To this aim we have evaluated the effects of an acute inhibition of angiotensin converting enzyme by enalapril (E). The renal function was explored by clearance (cl.) method during induced hypotonic polyuria (oral water load followed by 5% dextrose solution infusion). During 60 min cl. period the urinary PGE2, 6-keto-PGF1 alpha and TxB2 were determined by RIA method. Each subject received paired studies, in absence and presence of E (10 mg administered per os 1 hour before the water load). Basal values of plasma renin activity (PRA) and urinary aldosterone (excreted during the 24 hours before the water load) were also determined by RIA method. This study protocol was applied in normal potassium balance (n = 6) and induced moderate potassium depletion (n = 6). This paper concerns the group in potassium depletion in both absence (D4) and presence of E (D4.E). Potassium depletion was induced by adaptation to a normal sodium (150 mmol/d) and low potassium (< or = 10 mmol/d) dietary intake combined to natriuretic treatment. The water and NaCl net losses were restored by 0.9% NaCl solution infusion. The cumulative potassium deficit achieved at the end of the depletive treatment was 214 +/- 54 mmol. This treatment induced significant decrease in basal plasma potassium concentration and increase in PRA without affecting urinary aldosterone and plasma sodium concentration.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Renal effects of the acute inhibition of angiotensin-converting enzyme. I. 2) Studies during moderate potassium depletion]. 129 6

We have investigated the relative roles of some renal prostanoids and angiotensin II in the hypokalemic renal dysfunction. To this aim we have evaluated the renal function in healthy women in induced potassium depletion of moderate degree before and after acute inhibition of cyclooxygenase (indomethacin, I) or angiotensin converting enzyme (enalapril, E). The renal function was explored by clearance (cl.) method during hypotonic polyuria induced by oral water load followed by 5% dextrose solution infusion; the urinary PGE2, 6-keto-PGF1 alpha and TxB2 were determined by RIA method. Potassium depletion was induced in 12 subjects by adaptation to low potassium (< or = 10 mmol/d) and normal sodium (150 mmol/d) dietary intake combined to natriuretic treatment. The water and NaCl net losses were restored by 0.9% NaCl solution infusion. In 6 subjects paired functional studies were performed in absence (D3) and presence of I (D3.I), 100 mg administered i.m. immediately before the water load. In other 6 subjects, paired studies were performed in absence (D4) and presence of E (D4.E), 10 mg administered per os 1 hour before the water load. No significant difference between D3 and D4 was observed as regards the potassium cumulative deficit as well as the basal values of plasma potassium concentration and plasma renin activity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Renal effects of the acute inhibition of angiotensin-converting enzyme. I. 3) Relative roles of angiotensin II and prostanoids in early hypokalemic dysfunction]. 129 7

Aminoacylproline hydrolase (EC 3.4.11.9) of guinea pig serum has been obtained as two apparently homogeneous isoforms. Dialyzed serum was chromatographed successively on Affi-gel blue, hydroxyapatite, DE-cellulose, phenyl-Sepharose, an affinity matrix for angiotensin converting enzyme and concanavalin-Sepharose. On the latter matrix, 68% of the enzyme activity was eluted with alpha-methyl mannoside at 10 and 100 mM, and 29% was eluted with alpha-methyl glucoside, 500 mM, at 56 degrees C. The two fractions ('biantennary' and 'high mannose' fractions, respectively) were concentrated and then chromatographed separately on Sephacryl S-200HR. Both fractions were eluted as expected for a globular protein of Mr 217,000. On SDS-PAGE, under reducing and non-reducing conditions, each of the concanavalin-Sepharose fractions was separated into two protein bands, Mr 89,000 and Mr 81,500. Each of the bands was found to be N-blocked when N-terminal amino acid sequencing was attempted. The reaction of the 'biantennary' fraction with the synthetic substrate Arg-Pro-Pro-[3H]benzylamide was characterized in part: Km 0.7 microM, kcat 124.6 min-1, kcat/Km 1.78.10(8) M-1 min-1. Hydrolysis of the substrate was strongly inhibited by bradykinin and those of its lower homologs that contain two adjacent proline residues. Cu2+ was strongly inhibitory. Co2+ at 30 microM activated the enzyme, as did Mn2+, Mg2+ and Ca2+ at higher concentrations. Sulfhydryl compounds, including captopril, inhibited the enzyme as did 1,10-phenanthroline. Iodoacetamide and N-ethylmaleimide had no effects, but 4-hydroxymercuribenzoate conferred a partial inhibition over a remarkably wide concentration range: 0.34-1400 microM. Amastatin and bestatin did not inhibit the enzyme. Aminoacylproline hydrolase of guinea pig serum appears to be a heterogeneous, glycosylated metallo-enzyme with a high affinity for bradykinin and related peptides in which the sequence Pro-Pro, Xaa-Pro-Pro or Xaa-Pro-Hyp is N-terminal.
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PMID:Purification and characterization of guinea pig serum aminoacylproline hydrolase (aminopeptidase P). 154 Jun 46

The antihypertensive effect and tolerability of enalaprilat, an intravenously administered angiotensin converting enzyme inhibitor, was studied in 65 patients with moderate or severe hypertension. In this randomized, double-blind study, enalaprilat was compared with placebo in 42 (22 enalaprilat, 20 placebo) moderate hypertensive (diastolic blood pressure [BP] 100 to 114 mm Hg) patients. It was compared with furosemide in 23 (12 enalaprilat, 11 furosemide) severe hypertensive (diastolic BP 115 to 130 mm Hg) patients. Enalaprilat (1.25 or 5.0 mg), placebo (5% dextrose) or furosemide (40 or 80 mg) was given every 6 hours intravenously up to 48 hours. In the moderate hypertension stratum, the mean supine diastolic BP was significantly (p less than or equal to 0.01) reduced from baseline at all timepoints in the enalaprilat group. These diastolic BP reductions were significantly (p less than or equal to 0.01) greater in the enalaprilat group than the placebo at 1 to 24 hours (-12 vs -4 mm Hg), with 59% of the patients responding to enalaprilat compared with 30% of the patients responding to placebo. An even greater reduction (p less than or equal to 0.01) was seen at 25 to 48 hours (-14 vs -7 mm Hg, with 73% enalaprilat vs 58% placebo responders). Significant (p less than or equal to 0.01) reductions in mean, supine systolic BP were also seen at 1 to 24 hours (-22 vs -2 mm Hg) and 25 to 48 hours (-24 vs -8 mm Hg) during the 48 hours of the double-blind treatment phase in the enalaprilat group compared with placebo.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of intravenous enalaprilat in moderate and severe systemic hypertension. 284 22

Angiotensin converting enzyme (dipeptidyl carboxypeptidase, kininase II; EC 3.4.15.1), is a membrane bound glycoprotein, playing an important role in the renin-aldosterone system. The enzyme contains a carbohydrate moiety, consisting of fucose, mannose, galactose, N-acetylglucosamine and N-acetylneuraminic acid. Treatment with neuraminidase (EC 3.2.1.18) removes sialic acid from the molecule. The influence of this treatment on the electrophoretic mobility of the enzyme was studied in 29 human tissues and body fluids. Results obtained showed differences in the sialic acid content of the enzyme in the tissues examined.
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PMID:Influence of neuraminidase treatment on the electrophoretic behaviour of angiotensin converting enzyme from human tissues. 302 Jan 53

The leaves of the persimmon Diospyros kaki, have been traditionally used for treatment of hypertensive diseases in Japan. We have studied the inhibitory effects of four flavonoids isolated from the leaves of the persimmon on angiotensin-converting enzyme activity. The four flavonoids astragalin [1], kaempferol-3-O-(2"-O-galloyl)-glucoside [2], isoquercitrin [3], and quercetin-3-O-(2"-O-galloyl)-glucoside [4] inhibited the angiotensin-converting enzyme activity in a dose-dependent fashion. Compounds 1-4 produced 67%, 53%, 33%, and 48% inhibition at a concentration of 300 micrograms/ml, respectively. The 50% inhibitory concentrations (IC50) of 1 and 2 for the angiotensin-converting enzyme were 180 micrograms/ml and 280 micrograms/ml, respectively. On the other hand, 2 and 4 were shown to have tannin activities, but 1 and 3 had no tannin activities. These results suggest that there is no relationship between the inhibition for angiotensin converting enzyme activity and the tannin activity for the four flavonoids.
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PMID:Inhibitory effects of various flavonoids isolated from leaves of persimmon on angiotensin-converting enzyme activity. 343 Jan 65

The purpose of these experiments was to study the possible contribution of bradykinin to normal blood pressure maintenance. The bradykinin analogue B4146, a competitive antagonist-partial agonist of bradykinin, was used in three groups of normotensive unanesthetized Wistar rats. Two intra-aortic injections of B4146 (1 mg in 0.2 ml of dextrose) were given 5 minutes apart (i.e., well after return of blood pressure to baseline, which occurred within 68 +/- 19 seconds). One group had been pretreated with the angiotensin converting enzyme inhibitor HOE 498, 1 mg/kg (Hoechst), and one received only dextrose as the first injection to serve as controls. The bradykinin antagonist produced an average increase in mean arterial pressure of approximately 13 mm Hg for all groups. In five animals, however, the first injection of B4146 produced a hypotensive effect, whereas the second one consistently produced a rise in blood pressure. Pretreatment with the angiotensin converting enzyme inhibitor did not affect the magnitude of the subsequent blood pressure increase in response to B4146. Since smaller doses of B4146, sufficient to block exogenous bradykinin, do not cause changes in normal blood pressure, we conclude that endogenous bradykinin does contribute to normal blood pressure maintenance, but its effect can be demonstrated only if very high doses of its antagonist are injected, maybe because a high concentration of the compound is necessary to displace not only circulating but possibly tissue receptor-bound bradykinin as well.
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PMID:Hypertensive effect of a bradykinin antagonist in normotensive rats. 377 Aug 70


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