Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P00790 (PGA)
 2,475 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Immunoreactive (IR) plasma prostaglandin (PG) levels were measured in samples collected simultaneously through catheters placed in the right ventricle and the thoracic aorta in fasting anesthetized dogs. There were significantly greater levels of IRPGB (P less than .01) and IRPGA (P less than .05), but significantly less IRPGE (P less than .01) in the aorta than in the ventricle. During femoral vein infusion of PGE1, PGB1, and PGA1, respectively, PGE1 was approximately 87% metabolized, but PGB1 and PGA1 were not degraded by the lung. There was no measurable increase in IRPGB or IRPGA levels in the thoracic aorta during intravenous PGE1 infusion. It was concluded that in the resting state PGE is actively degraded by the lung; that the lung very effectively degrades PGE1 but does not degrade PGB1 or PGA1 during infusion of these prostaglandins; and that pulmonary metabolism of PGE1 probably does not result in formation and release of PGB or PGA into the arterial circulation. Additionally, the possibility exists that in the resting state PGB and/or PGA are actively secreted by the lung, but the immunoassay methodology used does not permit resolution of this point.
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PMID:Differential in vivo pulmonary degradation of prostaglandins E1, B1, and A1. 114 29

The effects of intrarenal infusion of prostaglandins (PGs) of the E, A and F series on renal vascular resistance and on vasoconstrictor responses to renal nerve stimulation (RNS), norepinephrine (NE) and angiotensin (A) were determined in the in situ feline kidney under conditions of controlled blood flow. Infusion of PGE2 (3 and 0.3 mug/min) and PGE1 (3 mug/min) resulted in a marked decrease in renal perfusion pressure and a reduction in responses to all vasoconstrictor stimuli. PGE2 (0.03 mug/min) did not alter perfusion pressure. However, responses to RNS and A but not to NE were attenuated. PGA2 (3 and 0.3 mug/min) had no significant effect on perfusion pressure. PGA1 (3 mug/min) resulted in a transient decrease in renal vascular resistance which was not maintained during the infusion period. PGA2 (3 mug/min) reduced the response to RNS at 10 and 30 cps and reduced the response to A, whereas responses to NE were not affected. PGA2 (0.3 mug/min) had no effect on responses to either of the pressor stimuli. PGA1 infusion resulted in an enhanced response to RNS at the highest stimulus frequency and decreased the response elicited by A. PGF2alpha (3 mug/min) had no significant effect on renal vascular resistance or on responses to NE and nerve stimulation. However, the response to angiotensin was decreased and responses to RNS at 10 and 30 cps were decreased 30 minutes after the PGF2alpha infusion. The present data demonstrate that, of the natural renal PGs, PGE2 and PGA2 possess the capacity to modulate the effects of the sympathetic nervous system on the feline kidney. In addition, the effects of PGE and PGA on responses to adrenergic stimuli and on vascular resistance could be separated.
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PMID:Influence of prostaglandins E, A and F on vasoconstrictor responses to norepinephrine, renal nerve stimulation and angiotensin in the feline kidney. 124 15

Two novel prostaglandins (PG) have been found in human seminal fluid which had been frozen immediately after collection. They were characterized by combined gas-liquid chromatography-mass spectrometry of various derivatives as 19-hydroxy prostaglandin E1 (11, 15, 19-trihydroxy-9-ketoprost-13-enoic acid) and 19-hydroxy prostaglandin E2 (11, 15, 19-trihydroxy-9-ketoprosta-5, 13-dienoic acid). They were present in three to five times the quantity of prostaglandins E1 and E2. Incubation of seminal fluid for 3 hr at 25 degrees C reduced levels of 190H-PGEs2.5-fold and PGE22-fold, while increasing levels of PGAs and PGBs 2-fold. No 190H PGA or 190H PGB was detected in extracts of unincubated fluid. The PGAs, PGBs and their 19-hydroxy analogs are probably artifacts arising metabolically or as a result of classical isolation techniques.
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PMID:11, 15, 19-trihydroxy-9-ketoprost-13-enoic acid and 11, 15, 19-trihydroxy-9-ketoprosta-5, 13-dienoic acid in human seminal fluid. 125 16

Liver fatty acid binding protein (L-FABP) is the principal target protein of the hepatic carcinogen N-(2-fluorenyl)acetamide (2-acetylaminofluorene) in rat liver. In addition, the cyclopentenone prostaglandins (PG), PGA, PGJ2, and delta 12-PGJ2, inhibit the growth of many cell types in vitro. This report describes the preferential binding of the growth inhibitory prostaglandins by L-FABP and the reversible inhibition of thymidine incorporation into DNA by PGA2 and delta 12-PGJ2 in primary cultures of purified rat hepatocytes. As a model ligand, [3H]PGA1 bound to L-FABP specifically, reversibly, rapidly, and with high affinity. Its dissociation constants were 134 nM (high affinity) and 3.6 microM (low affinity). The high-affinity binding of [3H]PGA1 was 9- and approximately 13-fold more avid than the binding of the conventional fatty acid ligands, oleic acid and arachidonic acid, respectively. The abilities of different prostaglandins to compete with the high-affinity binding of [3H]PGA1 correlated with their growth inhibitory activities reported previously and here. The growth inhibitory cyclopentenone prostaglandins (PGA1, PGA2, delta 12-PGJ2, and PGJ2) were the best competitive ligands, intermediate competitors were the weak growth inhibitors PGE1 and PGD2, and the poorest competitors were PGE2 and PGF2 alpha, which stimulate rather than inhibit DNA synthesis in rat hepatocytes in primary culture. The in vitro actions of L-FABP are compatible with those of a specific and dissociable carrier of growth inhibitory prostaglandins in rat hepatocytes and suggest that the carcinogen may usurp the cellular machinery of the growth inhibitory prostaglandins.
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PMID:Preferential binding of growth inhibitory prostaglandins by the target protein of a carcinogen. 225 Dec 82

Misoprostol, a prostaglandin E1 analogue was administered orally to male volunteers in doses of 50, 100, 200 and 400 mcg and its effects on gastric secretion compared with those observed following placebo. All doses significantly inhibited basal acid secretion by up to 98% and also inhibited histamine-stimulated secretion during the first 60 minutes of stimulation. Only the 50 mcg dose did not cause a significant reduction in acid output over the entire 2 hour period of histamine stimulation. The effect on gastric secretory volume was much less than that on acid, and in general the reductions were not statistically significant. Pepsin concentration was reduced during basal secretion only. Misoprostol is a potent inhibitor of basal acid secretion and moderately inhibits histamine-stimulated acid secretion with a duration of action of at least three hours following drug ingestion.
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PMID:Effects of misoprostol on histamine-related gastric secretion in man. 252 Aug 47

The profile of urinary metabolites of 3H-arbaprostil was characterized in the male dog after intravenous administration. The major metabolites were purified and their structures deduced by gas chromatography/mass spectrometry (GC/MS) studies after conversion to the methyl ester-methoxime-trimethylsilyl ether derivatives, aided by GC with simultaneous radioactivity monitoring. The identified metabolites accounted for 96% of the urinary excretion products. beta-Oxidation of the carboxy side-chain of arbaprostil to 15-methyl-2,3,4,5-tetranor PGE1, via the 15-methyl-2,3-dinor PGE2 intermediate, appeared to be the most significant metabolic pathway. In contrast to the rat, the following were observed in the dog: glucuronic acid conjugation of the 15-methyl-2,3,4,5-tetranor PGE, and PGA metabolites; detection of the 15-methyl-2,3-dinor PGE2 intermediate; absence of 19-hydroxyl-15-methyl-2,3,4,5-tetranor PGA, and PGB metabolites; oxidation at C-20; and excretion of some parent drug.
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PMID:Isolation and characterization of the urinary metabolites of arbaprostil in the male dog after intravenous administration. 320 90

Human umbilical blood vessels have the ability to close spontaneously following delivery at term. It has been suggested that prostaglandins may have a possible physiological role in its closure. This study investigates the effects of 6 naturally occurring prostaglandins (A1, A2, B1, B2, E2, F2a) on the umbilical blood vessels. Umbilical cords were collected from cases of normal spontaneous vaginal deliveries and cesarian section at term. A total of 41 strips of umbilical arteries and 26 strips of umbilical veins from 24 cords were used. A 4-point bioassay method was used to compare the potency of prostaglandins A1, A2, B1 and F2a with PGE2. The effect of Polyphloretin Phosphate (PPP) on prostaglandin-induced contractions was studied on umbilical artery strips from 12 cords. The 6 prostaglandins exerted a stimulant effect on the isolated strips of human umbilical arteries. Prostaglandin B2 was the most potent compound on the umbilical vein, followed by PGA2. PPP in the concentration range of 10 to 40 mcg/ml completely eliminated the responses of PGE2, F2a, A1, A2, and B1. Responses to PGB2 were considerably but not completely abolished. PPP (up to 40 mcg/ml) did not affect contractions induced by 5-hydroxytryptamine, suggesting the presence of discrete receptor sites in the blood vessels for different pharmacologically active compounds. This is the first report of the constrictor effect of PGA and PGB compounds. These naturally occuring prostaglandins with high potencies (compared with other prostaglandins and other vasoactive substances) may play a role in spontaneous closure of umbilical vessels. PGE1, E2, F1 and F2a are found in umbilical blood vessels obtained at term.
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PMID:Effect of prostaglandins A1, A2, B1, B2, E2 and F2 alpha on human umbilical cord vessels. 445 25

Antibodies to the (PGA) prostaglandin A were produced in rabbits immunized with a conjugate of PGE2 covalently linked to (BSA) bovine serum albumin by reaction with carbodiimide reagent. A radioimmunoassay was developed using dextran-coated charcoal to separate the free from antibody bound PGA1-3H. The sensitivity of the method was found to be 100 picograms/ml of plasma. Ethyl acetate was used for extraction of plasma and the various classes of PGs were separated by silicic acid column chromatography. Recovery of PGA1-3H throughout the entire procedure was 65-75%. The antibody showed progressively decreasing affinity to PGA2, PGA1, PGE2, PGE1, PGB2, and PGF2alpha, respectively. The mean plasma PGA level in adult males (N=13) was found to be 1.39 + or - 0.55 ng/ml, and 1.62 + or - 0.52 ng/ml in adult females (N=7). Corresponding plasma and serum samples were found to give essentially similar results. Plasma PGA levels in adult males treated with indomethacin for rheumatoid arthritis were 0.18 + or - 0.15 ng/ml (P 0.001 in comparison with the normal adult males). This method is sufficiently sensitive, precise, and rapid to allow the routine estimation of the PGAs in biological samples.
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PMID:Radioimmunoassay of the A prostaglandins. 466 56

The procedures which may be and are being used to provide a basis for the analysis of submicrogram quantitities of prostaglandins are surveyed. Discussion is focused on the following: 1) sources of standards; 2) properties (effect of different pH values, effect of blood, metabolism, solubility); 3) extraction; 4) detection; 5) estimation (ultraviolet, optical rotatory dispersion, densitometry, radioimmunoassay, enzymatic assay, isotopic methods, bioassay); 6) separation of prostaglandins (separation of PGE, PGF, and PGA with PGB compounds, separation of PGA and PGB compounds, and separation of individual prostaglandins); and 6) structural identification. Methods of prostaglandin analysis, with the required sensitivity for application to individual tissue and fluid specimens, are still in the developmental state. Although prostaglandins may be ubiquitous throughout the animal kingdom, no systematic study of their distribution has been made to date. Recent work has shown that PGE1 has a potent effect on the formation of 3',5' cyclic adenosine monophosphate (cyclic AMP) which is widely believed to be an intracellular intermediate in hormone action.
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PMID:Separation, identification, and estimation of prostaglandins. 489 63

Antibodies to prostaglandin were obtained by immunization of rabbits with PGA(1), PGA(2), and PGE(1), protein conjugates of prostaglandins. The antibodies demonstrated specificity toward both the cyclopentane ring and the aliphatic side chains. With the use of these antibodies a highly sensitive radio-immunoassay capable of measuring less than picomolar amounts of PGA1, PGA2, and PGE1 has been developed.
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PMID:Radioimmunoassay for prostaglandins. 553 3


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