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)

Electrolyte abnormalities are a frequent and potentially hazardous complication in patients with heart failure. This may be due to the pathophysiological alterations seen in the heart failure state leading to neurohumoral activation (stimulation of the renin-angiotensin-aldosterone system, sympathoadrenergic stimulation), and due to the complications of therapy with diuretics, cardiac glycosides or ACE inhibitors. Patients with heart failure may exhibit hyponatremia due to a decrease in water excretion, which may be related to the enhanced release of both angiotensin and vasopressin and can be exaggerated by diuretic therapy. Along with potassium and calcium, magnesium influences cardiovascular function. Magnesium and potassium deficiencies play an important role in the development of cardiac arrhythmias. Magnesium is essential for the maintenance of intracellular potassium concentration. Although there are conflicting data regarding the prevalence of hypomagnesemia in patients with chronic heart failure (the values range from 7-37%), multiple studies have documented lower magnesium concentrations in patients with heart failure than in normal controls. As magnesium and potassium are mainly intracellular ions, measurements in serum or plasma are of limited value to assess magnesium status. There was no correlation between the intracellular electrolyte content and the electrolyte levels in plasma, either for mononuclear cells or erythrocytes or for myocardial and skeletal muscle. Loop diuretics (e.g. furosemide) are supposed to cause a substantial loss of both magnesium and potassium in the plasma and intracellular space. The potassium-sparing diuretics amiloride and triamterene are reported to also exert magnesium-sparing effects. Recently, ACE inhibitors have been documented to have important magnesium-conserving actions, possibly via their effect on glomerular filtration. Hyperkalemia, secondary to the use of ACE inhibitors in patients with heart failure, is well documented. Digoxin directly limits the renal tubular reabsorption of magnesium, therefore increasing magnesium excretion. Low magnesium and potassium concentrations increase cardiac glycoside toxicity. In contrast, elevated levels of magnesium decrease the sensitivity of human myocardium to antiarrhythmogenic actions of cardiac glycosides, without affecting maximally developed tension. Moreover, magnesium increases binding affinity of cardiac glycosides to the receptor. The antiarrhythmic action of magnesium is suspected to be mediated by a reduced sensitivity to electrophysiological changes induced by Ca2+, thus indicating Ca2+ antagonistic properties of magnesium. Magnesium deficiency has also been implicated in sudden death, notably in patients with congestive heart failure. Therefore, when treating congestive heart failure, one must consider how to prevent depletion of electrolytes or how to replete potassium and magnesium in deficiency states.
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PMID:Heart failure and electrolyte disturbances. 150 35

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 renal responses of magnesium lithospermate B were investigated in the presence or absence of pretreatment with the converting enzyme (kininase II) inhibitor, captopril, in rats with adenine-induced renal failure. Magnesium lithospermate B (10 mg/kg body weight) caused a marked increase in the levels of the renal functional parameters (glomerular filtration rate, renal plasma flow and renal blood flow), accompanied by significant increases in urinary excretions of prostaglandin E2 (PGE2), kallikrein, sodium and creatinine. The administration of magnesium lithospermate B in combination with captopril (2 mg/kg body weight, 2 times) caused a further increase in renal functional parameters, urinary sodium and creatinine excretions. However, the kallikrein activity was similar to the control level. There were no significant changes between urinary PGE2 following magnesium lithospermate B alone, or in combination with captopril. In addition, angiotensin converting enzyme activity did not change following the administration of magnesium lithospermate B alone, but was significantly decreased in rats given captopril, both alone and in combination with magnesium lithospermate B. The captopril administration group (captopril alone or in combination with magnesium lithospermate B) showed a significant decrease in blood pressure. From these results, it seems that the combination of magnesium lithospermate B and captopril induces a further increase in renal function by improving the renal circulatory state.
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PMID:Potentiating effect of converting enzyme inhibitor captopril to the renal responses of magnesium lithospermate B in rats with adenine-induced renal failure. 207 Apr 57

Both angiotensin converting enzyme (ACE) inhibition and sodium-diuresis lower blood pressure in spontaneously hypertensive rats (SHR). The purpose of the present study was to examine whether long-term therapy with ramipril (RA, and ACE inhibitor) would lower blood pressure more effectively and without adverse reactions in combination with the loop diuretics piretanide (PI) or furosemide (FU). Groups of 15 SHR each were treated once daily for 3 weeks by gavage with 1 and 10 mg/kg RA, 2 and 4 mg/kg PI, and 8 and 16 mg/kg FU alone and with 1 mg/kg RA in combination with each of these diuretics at both the high and low doses. Sustained and marked ACE inhibition with 10 mg/kg RA normalized BP, but this was accompanied with slightly impaired kidney function as assessed by increases in both urea and creatinine. Low-dose diuretic therapy, producing little diuresis, or treatment with 1 mg/kg RA, producing less sustained ACE inhibition were less effective on blood pressure and scarcely altered serum solute levels, except 4 mg/kg PI, which produced slight reductions in Na+, K+, Mg2+, and PO4(3-). Combined treatment with the 1 mg/kg RA with either diuretic given at low or high dose was well tolerated at much improved reduction in blood pressure compared to their effects individually and without changes in serum solute concentrations and without hemoconcentration. Thus, combined treatment with low doses of loop diuretics and ACE inhibitors that permit partial recovery of serum ACE activity during the 24 h after dosing synergistically lowers blood pressure without adverse reactions associated with larger doses of either therapy alone.
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PMID:Loop diuretics combined with an ACE inhibitor for treatment of hypertension: a study with furosemide, piretanide, and ramipril in spontaneously hypertensive rats. 247 99

In vivo administration of L-thyroxine (L-T4) in Anabas testudineus, while significantly stimulated the activities of cytochrome c oxidase and alpha-glycerophosphate dehydrogenase (alpha-GPDH), inhibited glucose-6-phosphate dehydrogenase (G-6-PDH), cytosolic and mitochondrial malate dehydrogenase (cyt. MDH; mit. MDH), and Mg2+ DNP-dependent adenosine triphosphatase (Mg2+ ATPase) activities. The activities of lactate dehydrogenase (LDH), succinate dehydrogenase (SDH), and catalase remained unaltered after L-T4 treatment. Administration of protein synthesis inhibitors such as actinomycin D, while significantly inhibited cytochrome oxidase, alpha-GPDH, catalase, SDH, and Mg2+ ATPase activities, did not change LDH, cyt. MDH, and mit. MDH activities. Chloramphenicol injection significantly stimulated cytochrome oxidase, alpha-GPDH, and G-6-PDH activities. Simultaneous injections of actinomycin D or chloramphenicol with 3,5,3'-triiodo-L-thyronine (L-T3) or L-T4 prevented the effects of thyroid hormones on enzyme activities, when compared to the respective controls.
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PMID:Oxidative metabolism in a teleost, Anabas testudineus Bloch: effect of thyroid hormones on hepatic enzyme activities. 292 Sep 3

1. The in vivo and in vitro conditions which allow a response of rat circulating lymphocyte PDH to insulin are investigated. 2. In vivo tests show that inactive PDH (PDHi) prevails in diabetic rats and active PDH (PDHa) in hyperinsulinemic rats; in treated with insulin diabetic rats the PDHa/PDHi ratio (1.7) is similar to that of normal rats (PDHa/PDHi ratio = 2). 3. In vitro tests show a responsiveness of PDH to insulin only when 50 microM Ca2+ -Mg2+ and intact lymphocytes are used in the incubation medium. Insulin concentrations and contact time are important variables.
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PMID:Effects of insulin on pyruvate dehydrogenase in circulating lymphocytes from normal and diabetic rats. 305 85

Mobility of phospholipid hydrocarbons in the Escherichia coli B membrane fractions was studied by labeling phosphatidylethanolamine or phosphatidylglycerol in situ by biosynthetic incorporation of the spin label. For this purpose, CDP-diacylglycerol spin label was synthesized from phosphatidic acid spin label and cytidine 5'-phosphoromorpholidate and purified by thin-layer chromatography. DCP-diacylglycerol spin label was then incorporated into phospholipids biosynthetically. ESR spectra of these E. coli B membrane fractions showed that phosphatidylglycerol tended to interact with membrane proteins through the mediation of Mg2+, whereas phosphatidylethanolamine had less of this tendency and was more involved in the formation of the bulk of the bilayer continuum of the membrane. These conclusions were also supported by labeling membranes with exogenous spin-labeled phospholipids, although there was some indication that exogenous phospholipids were incorporated into sites different from the sites of incorporation of phospholipids newly synthesized in situ.
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PMID:Dynamic states of phospholipids in Escherichia coli B membrane. Electron spin resonance studies with biosynthetically generated phospholipid spin labels. 626 61

The role of calcium regarding the origin of irreversible impairment of the myocardial tissue is being intensively studied. An important role in this process is played by mitochondria which by means of the active Ca2+ uptake stimulate its oxidative metabolism and intervene into the Ca2+ homeostasis in mitochondrial cells. The study investigates the influence of cardioprotective substances with distinct mechanisms of the mitochondrial Ca2+ uptake effect. The experiments were performed on chinchilla buck rabbits of 2500-3000 g of body weight. Isolated hearts were perfused according to the method of Langendorff, ischemia was evoked by a 60-minute stoppage of the coronary blood flow. The cardioprotective substances were added into the perfusion solution prior to ischemia inducement. We investigated the following cardioprotective substances: Spirapril (ACE inhibitor), magnesium (Mg2+), and MDL 73,404 (antioxidant, synthetic analogue of alpha-tocopherol). After the 60-minute ischemy the mitochondrial Ca2+ uptake decreased by 43% in comparison with the control group (p < 0.01), Spirapril caused its accretion by 35% in comparison with the ischemic group (p < 0.05), and magnesium increased the uptake even by 52% (p < 0.001). The MDL 73,404 substance had no effect on the mitochondrial Ca2+ uptake. On the basis of experimental results we assume that the cardioprotective effects of Spirapril and magnesium can be besides other factors intermediated also by the increase of intramitochondrial enzymatic activity in consequence of augmented transport of Ca2+ into mitochondria. The cardioprotective effect of the MDL 73,404 substance is assumedly caused by its antioxidant properties. (Fig. 4, Ref. 21.)
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PMID:[Significance of mitochondrial Ca2+ transport in ischemic injury and myocardial protection]. 781 44

Thirty-six feed phosphates, including nine mono-dicalcium phosphates (M-DCP, 21% P), 13 di-monocalcium phosphates (D-MCP, 18.5% P), and 14 thermochemically produced defluorinated phosphates (DFP, 18.0% P), were analyzed for moisture, Ca, P, and 9 essential minerals (K, Mg, Na, Cl, Fe, Cu, Mn, Se, and Zn). Also, nine potentially toxic elements (Al, F, As, Cd, Cr, Hg, Pb, Ni, and V) were determined. All of the M-DCP were of domestic origin; 5 of the 13 D-MCP samples were obtained in Algeria, Peru, Holland, and South Africa. The DFP samples included 10 domestic products, 2 samples from Russia, 1 from Poland, and 1 from Japan. Levels of Na were high in the DFP samples (3.96 to 5.78%), except for the two Russian samples, which contained only .16 and .19%. Magnesium levels varied from .09 to .76%, .02 to 1.21%, and .01 to 1.54% in the M-DCP, D-MCP, and DFP samples, respectively. Two Russian DFP samples contained 1.51 and 1.54% Mg. Chlorine levels were generally quite low (.002 to .020%); however, two precipitated D-MCP samples contained .12 and 1.47% Cl. Iron levels were high (.24 to 1.41%) in all samples except the bone-precipitated D-MCP (.039%), and the reference standard, calcium phosphate, dibasic dihydrate, USP (.029%). Levels of Cu, Mn, and Zn were quite variable. Cadmium varied from < 1 ppm in the DFP samples to 67 ppm in one experimental M-DCP. Vanadium levels varied from 20 to 796 ppm in one experimental M-DCP sample. Fluorine levels were in the acceptable range, .05 to .21%.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Levels of various elements of concern in feed phosphates of domestic and foreign origin. 820 31

Angiotensin-converting enzyme (ACE; EC 3.4.1.15.1) exists in both membrane-bound and soluble forms. Phase separation in Triton X-114 and a competitive e.l.i.s.a. have been employed to characterize the activity which post-translationally converts the amphipathic, membrane-bound form of ACE in pig kidney microvilli into a hydrophilic, soluble form. This secretase activity was enriched to a similar extent as other microvillar membrane proteins, was tightly membrane-associated, being resistant to extensive washing of the microvillar membranes with 0.5 M NaCl, and displayed a pH optimum of 8.4. The ACE secretase was not affected by inhibitors of serine-, thiol- or aspartic-proteases, nor by reducing agents or alpha 2-macroglobulin. The metal chelators, EDTA and 1,10-phenanthroline, inhibited the secretase activity, with, in the case of EDTA, an inhibitor concentration of 2.5 mM causing 50% inhibition. In contrast, EGTA inhibited the secretase by a maximum of 15% at a concentration of 10 mM. The inhibition of EDTA was reactivated substantially (83%) by Mg2+ ions, and partially (34% and 29%) by Zn2+ and Mn2+ ions respectively. This EDTA-sensitive secretase activity was also present in microsomal membranes prepared from pig lung and testis, and from human lung and placenta, but was absent from human kidney and human and pig intestinal brush-border membranes. The form of ACE released from the microvillar membrane by the secretase co-migrated on SDS/PAGE with ACE purified from pig plasma, thus the action and location of the secretase would be consistent with it possibly having a role in the post-translational proteolytic cleavage of membrane-bound ACE to generate the soluble form found in blood, amniotic fluid, seminal plasma and other body fluids.
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PMID:Characterization of a secretase activity which releases angiotensin-converting enzyme from the membrane. 838 41


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