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At least 19 recordsLinked to original sources
PubMed1985

Determination of immunoreactive antiarrhythmic peptide (AAP) in rats.

A sensitive and specific radioimmunoassay for antiarrhythmic peptide (AAP) has been developed, utilizing 3-(4-hydroxy, 5-[125I]iodophenyl)propionyl AAP and guinea pig anti-AAP serum. Synthetic AAP was used as a standard and the polyethylene glycol method was employed to separate free AAP from antibody-bound AAP. The minimum detectable dose of AAP was 0.2 pmol. In the assay system, immunoreactivity was shown not to be attributable to fragments derived from AAP, gelatin or collagen peptides, which sequences differ only by one amino acid from those of AAP. Immunoreactive (IR) AAP extracted from rat tissues and serum gave parallel dose-response curves to those of AAP. Thus, the AAP equivalents per g or ml of tissues measured in adult male rats were 203 pmol in heart, 166 pmol in kidney, 4 pmol in serum, and 2 to 6 pmol in the other tissues. IR-AAP was separated into two fractions by Sephadex G-25 chromatography. Fr. I was considered to have a larger molecular mass than AAP, while Fr. II appeared to have a molecular mass equal to AAP. Ratios of Fr. II in total IR-AAP were 50% in heart and 10% in kidney, while serum IR-AAP gave only Fr. II. The IR-AAP level in heart showed a positive correlation increase with age in rats.

Animals↗
PubMed1991

[Clinical evaluation of urinary alanine aminopeptidase in the patients with diabetes mellitus-comparison among AAP microalbumin and N-acetyl-beta-D-glucosaminidase].

To determine whether or not urinary Alanine aminopeptidase (AAP) could be used as an early marker for diabetic nephropathy, urinary AAP, microalbumin and N-acetyl-beta-D-glucosaminidase (NAG) were measured in 132 diabetic patients and 59 normal subjects. Urinary AAP, microalbumin and NAG in the diabetic patients and the normal subjects were 15.5 +/- 11.7 U/g. Cr and 9.1 +/- 6.9 (P less than 0.01), 27.4 +/- 35.5 mg/g. Cr and 8.4 +/- 4.4 (P = 0.0001), 10. 3 +/- 9.5 U/g. Cr and 3.9 +/- 2.1 (P = 0.0001), respectively. AAP had a moderate correlation with NAG (r = 0.58, P = 0.0001). AAP, microalbumin and NAG showed a slight positive correlation with age (AAP: r = 0.25, P less than 0.01, microalbumin: r = 0.32, P less than 0.01, NAG: r = 0.21, P less than 0.05), although it is significant, and AAP had a positive correlation with urinary protein concentration (r = 0.45, P = 0.0001) in diabetic patients. However, AAP in diabetic patients without proteinuria was higher than that in age-matched normal subjects. Urinary AAP was correlated with the indices of renal tubular damage like NAG, alpha 1-microglobulin and beta 2-microglobulin, so it seemed to be tubular origin but in the patients with clinical proteinuria, it might be partially glomerular origin. Since urine AAP increased in some patients without microalbuminuria and was not influenced by control of blood sugar, AAP could be used as an early marker of diabetic nephropath y in addition to microalbumin and NAG, but the effect of age should be considered in its estimation as in the case of NAG.

Acetylglucosaminidase↗
PubMed1986

Response of immunoreactive antiarrhythmic peptide (IR-AAP) level associated with experimental arrhythmia in rats.

The change in endogenous antiarrhythmic peptide (AAP) levels in serum, heart and kidney from rats under several drug-induced arrhythmias was investigated using a sensitive and specific radioimmunoassay. The extracts from serum, heart and kidney were fractionated by Sephadex G-25 chromatography to obtain a fraction which was found at the same position as that of synthetic AAP. In serum, the immunoreactive (IR)-AAP level increased about threefold under CaCl2-, aconitine- and epinephrine-induced arrhythmias. In heart, the IR-AAP level was doubled by CaCl2, increased 1.4 times by aconitine and decreased by one third by epinephrine. The levels in serum and heart were slightly increased by ADP. The kidney IR-AAP level was not changed under these drug-induced arrhythmias. Considering the previous result that AAP could protect against CaCl2- and aconitine-induced arrhythmias but not against epinephrine-induced arrhythmia, the change in the IR-AAP level in heart coincided with the effect of AAP given to animals under arrhythmia. Quinidine, propranolol and verapamil had no effect on serum IR-AAP level. These results suggested that endogenous AAP in heart worked to suppress certain arrhythmia.

Aconitine↗
PubMed1986

Potent platelet antiaggregant action of an antiarrhythmic peptide (AAP).

A potent platelet antiaggregant action of an antiarrhythmic peptide (AAP) was demonstrated to be a cause of the antithrombotic effect. AAP (10, 20 or 40 mg/kg, i.v.) inhibited ex vivo platelet aggregation induced by collagen in a dose-dependent manner. AAP also inhibited the platelet aggregation of platelet-rich plasma (PRP) induced by collagen, Ca-ionophore A-23187, adenosine diphosphate (ADP), thrombin or arachidonic acid in vitro. The IC50 was 2.5 mM for collagen, 1.7 mM for A-23187, 5 mM for ADP, 0.4 mM for thrombin and 0.15 mM for arachidonic acid. The aggregation inhibitory activity of the peptide on washed platelet (WP), in a Ca2+-free medium, was stronger than on PRP. The IC50 was 1 mM for collagen and 20 microM for A-23187. No significant difference was found between antiaggregant activities of platelet-free plasma (PFP) from AAP-treated rats and PFP from normal rats supplemented with AAP. The direct action of AAP on platelets was also supported by the incorporation of AAP into platelet cytoplasma which caused a decrease of Ca2+-dependent 3':5'-cyclic nucleotide phosphodiesterase (Ca-PDE) activity. It was considered that AAP showed its platelet aggregation inhibitory activity by decreasing intracellular Ca2+ concentration through the inhibition of Ca-PDE activity.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1991

Enzyme activities of urinary alanine aminopeptidase (AAP) and N-acetyl-beta-D-glucosaminidase (NAG) in healthy dogs.

The activity of the urinary enzymes alanine aminopeptidase (AAP; EC 3.4.11.2) and N-acetyl-beta-D-glucosaminidase (NAG; EC 3.2.1.30) was measured after eliminating distorting factors in ten healthy dogs on three consecutive days in order to determine inter- and intra-individual variability. All the animals were being housed and fed in the same way. The urine (2nd morning urine) was collected between 8:30 and 10:00 a.m. by means of ultrasound-controlled cystocentesis. Our comparative measurements of native and gel-filtered urine showed an increase in enzyme activity in all of the samples in the case of AAP and in most of the samples in the case of NAG, thus proving the existence in the dog of AAP and NAG urinary enzyme inhibitors. The large inter- and intra-individual AAP and NAG fluctuation ranges were reduced considerably by relating enzyme activity to urine creatinine concentration. The provisional upper limit of the AAP reference range is 6.3 U/g creatinine (90% percentile), that of NAG 6.2 U/g creatinine (90% percentile). The AAP and NAG enzyme activities remained constant in gel-filtered samples kept at 4 degrees C for at least 5 days, in those kept at -18 degrees C for at least 4 weeks.

Acetylglucosaminidase↗
PubMed1988

Urinary alanine-aminopeptidase (AAP) excretion in patients with urinary tract infection treated with ceftazidime (CAZ) or cefotaxime (CTX) plus tobramycin (TOB).

It is well known that some antibiotics are particularly nephrotoxic. In the present study we investigated kidney function and AAP excretion (as an index of nephrotoxicity) in patients with urinary tract infection treated with CAZ or CTX plus TOB. The main cause of infection was E. coli in both treated groups. After 10 days of treatment similar beneficial effects were stated in both groups. At the end of treatment urinary AAP excretion in both groups was higher than before treatment. Despite a significant increase in urinary AAP in only one patient of each group, the serum creatinine level rose by more than 45 mumol/l. Monitoring of urinary AAP may be useful in early detection of nephrotoxicity caused by antibiotics.

Adult↗
PubMed1975

[Isoenzymes of alanine arylamidase (AAP, EC 3.4.11.2) and gamma-glutamyltranspeptidase (GGTP, EC 2.3.2.2) in chronic pancreatitis and pancreas neoplasm (author's transl)].

In 22 patients with chronic pancreatitis and 16 patients with pancreas neoplasms gamma-glutamyltranspeptidase (GGTP) and alanine arylamidase (AAP) in serum were measured and the isoenzymes were determined by gel electrophoresis on Agar. No specific isoenzyme pattern was found for chronic pancreatic diseases in a comparative investigation with a group of 19 patients suffering from hepatobiliary diseases. Two fractions of AAP and GGTP isoenzymes were found on agar gel electrophoresis: alpha-1 and alpha-2 (GGTP between alpha-2 and beta-globulin). The alpha-1 fraction of AAP and GGTP seems to be a specific liver isoenzyme. The slower fraction of both enzymes was also found in chronic pancreatic diseases and cholestatic diseases as in neoplasms of liver, pancreas and biliary tract. Practical importance of the findings is diminished by large variation coefficients of the results. A significantly low ratio of alpha-1 to alpha-2 fraction (or beta-globulin) on electrophoresis of the isoenzymes of AAP and GGTP was found in the group with neoplasm of pancreas (especially neoplasm of the pancreas head) as compared to the group with intrahepatic cholestasis. The possible causes and diagnostic importance of the findings are discussed.

Alanine↗
PubMedDate not supplied

[Neonatal hypoxic-ischemic nephropathy and urinary diagnostic indices: the utility of measuring tubular enzymes (NAG and AAP)].

Feto-neonatal hypoxia can cause a functional kidney impairment, which is often temporary and not clinically overt, but sometimes leading to acute renal failure. Hypoxic stress may result in a tubulo-interstitial damage, and kidney tubular enzymes determination has proved to be an easy, early, and non invasive method to define a tubular interstitial lesion. A major target of nephrotoxicity is the proximal tubular cell: alterations in brush-border membrane and cytoplasm result in increased turnover processes in the kidney cortex, following by a corresponding increased excretion of alanine-aminopeptidase (AAP) and N-acetyl-glucosaminidase (NAG) from the proximal tubular cells, long before glomerular or tubular functions are impaired. AAP and NAG excretion is directly correlated with the strength and the duration of toxic alteration of the proximal tubule. NAG and AAP have been already studied in the adults and the children; they have been chosen for this investigation with a double aim: 1) to define the amount of their urinary excretion in relation with gestational age at birth; 2) to evaluate if in the newborn, independently of the gestational age, their urinary concentration may be increased by ischaemic conditions caused by hypoxia. We studied 52 healthy newborns (7 preterm of 33-36 weeks and 45 full-term) and 16 newborns with feto-neonatal hypoxia (8 preterm of 26-36 weeks and full-term) at the forth day of life. Urinary NAG and AAP were assayed by colorimetric methods and the results expressed as mU/mg. creatininuria.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylglucosaminidase↗
PubMed1989

[Clinical investigation of urinary activity of NAG and AAP in patients with various types of primary glomerulonephritis].

We investigated the activity of NAG and AAP in the urine of 36 patients with chronic glomerulonephritis (GN) with special reference to the relation between the levels of the enzymes and histopathological changes of the kidney. The subjects consist of 7 cases of minimal change nephrotic syndrome (MCNS), 3 cases of membranous GN, 5 cases of IgA. GN, 5 cases of membranoproliferative GN, 3 cases of focal glomerulosclerosis and 12 cases of chronic renal failure who had creatinine levels of more than 2 mg/dl resulting from chronic GN. Urinary levels of NAG and AAP were significantly higher in cases with GN than those in cases with chronic renal failure. In cases with GN, urinary levels of NAG and AAP correlated with the amounts of urinary protein, while those levels had no correlation with the classification of histopathological changes of glomeruli. The high value of NAG/mg.protein ratio, NAG by urinary protein, might be explained by the degree of tublointerstitial damage. We concluded that urinary levels of NAG and AAP reflects the proximal tubular damage caused by protein reabsorption.

Acetylglucosaminidase↗
PubMed1989

[Therapeutic effects and influence on the urinary enzyme activity of human urinary trypsin inhibitor (urinastatin) in cases with acute renal failure--changes in the urinary activities of NAG and AAP].

We studied the therapeutic effects of human urinary trypsin inhibitor (UTI) in 5 cases with acute renal failure, resulting from traumatic shock in 1 case, post-operative shock in 2 cases, septic shock in 1 case, and dehydration in 1 case. We administered 300,000 u/day of UTI intravenously at the initial phase of acute renal failure for 7 days. We measured the activities of urinary N-acetyl-beta-D-glucosaminidase (NAG), alanine aminopeptidase (AAP) and the activities of serum beta-glucuronidase, PMN-elastase serially. As a control, we also studied same markers in 5 cases with acute renal failure without the administration of UTI. We could obtain the following results. 1) Urinary activities of NAG and AAP were already elevated markedly at the onset phase of acute renal failure. 2) The administration of UTI caused a significant decrease of the activities of NAG and AAP in the urine as compared with those in the controls. 3) The administration of UTI caused also the significant suppression of the activities of beta-glucuronidase and PMN-elastase in the serum. These results suggested that UTI has the protective effects on the tubular epithelial cell injuries in cases of acute renal failure.

Acetylglucosaminidase↗
PubMed1989

[Evaluation of the liberation of urinary necrosis enzymes (NAG-AAP) after administration of plasma expanders: study of dextran 40, hydroxyethyl starch and polymerized gelatin].

We studied the 24-hour urinary elimination of enzymatic markers of renal tubular necrosis (NAG-AAP) in 21 patients (mean age 34.6 years old) who were treated with plasma expanders before peridural anesthesia. The patients were divided into three groups of seven subjects each: - 14 ml/Kg -1 of dextran 40 was administered to group 1 - 14 ml/Kg -1 of gelatin was administered to group 2 - 14 ml/Kg -1 of hydroxyethyl starch was administered to group 3. Urinary elimination of N-acetylglucosaminidase and of alanine aminopeptidase was determined in the 24-hour urine the day before surgery (controls), the day of surgery (G1) and the day after surgery (G2). The values of the samples, taken after plasma expander administration, did differ significantly from the control values (G1, G2). Therefore the administration of 14 ml/Kg -1 of dextran, gelatin or hydroxyethyl starch does not affect the renal tubular epithelium.

Acetylglucosaminidase↗
PubMed1989

Effects of progesterone and estradiol on aminopeptidase A (AAP) and leucine aminopeptidase (LAP) activities in the pregnancy serum and placenta of the rat.

We investigated the effects of estradiol and progesterone on placental aminopeptidase A and leucine aminopeptidase activities in pregnant rats. Estradiol (0.5, 1.0 and 2 mg/day) plus progesterone (5, 10 and 20 mg/day) was given for five days starting from the 16th day. Changes in both enzyme activities in the serum, placental cytosol and microsome caused by the steroids were analyzed. Aminopeptidase A activities in all three compartments and leucine aminopeptidase activities in the serum and cytosol were stimulated by estradiol (1.0 mg/day) plus progesterone (10 mg/day). Since we previously found that the placental aminopeptidases degrade peptide hormones, our present study suggests that steroids effect the metabolism of peptide hormones of fetal and/or maternal origin.

Aminopeptidases↗