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)

The effects of atropine on pentagastrin-stimulated gastric secretion of water, H, Cl, Na, K, and pepsin were determined by kinetic analysis of dose-response studies in 5 dogs with esophagostomy and gastric cannula. First a dose-response study was done using 7 doses of pentagastrin (1-6 mug/kg hr), each dose given by I.V. infusion for 4 hr at a separate time. The same series of doses was used with atropine sulfate 10 mug/kg hr as background. Atropine inhibited pentagastrin-stimulated secretion competively with a dose ratio change of 20. In a third set of studies pentagastrin was infused alone for 4 hrs in the dose of 1.5 mug/kg hr and then with each of 7 doses of atropine (0.625-40 mug/kg hr), each dose used separately. Atropine competitively inhibited water, H, Cl, and K secretion, with Ki (dose of atropine giving 50% inhibition) of 1.0 mug/kg hr. Pepsin secretion was much more strongly inhibited than acid secretion by atropine with Ki 0.27 mug/kg hr and the inhibition was uncompetitive. Calculated maximal inhibition of H+ secretion by atropine was 89% and of pepsin 95%. Furthermore the shape of the response to pentagastrin was altered by atropine so that the peak response was delayed to the third and fourth hour of pentagastrin infusion.
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PMID:Kinetics of atropine inhibition of pentagastrin-stimulated H+, electrolyte, and pepsin secretion in the dog. 31 59

The effect of the osmolarity of intragastric instillates on pepsin secretion was studied in rats anaesthetised with urethane. Irrigation of the stomach with solutions of sucrose and NaCl, resp. caused a concentration-dependent increase in pepsin output. A stimulation was observed already by hypotonic solutions and the maximal effect was obtained by 300 m-osmole/l of sucrose and by 600 m-osmole/l of NaCl (13- and 10-fold stimulation resp.). A similar time course in the increase of pepsin output was produced by hyperosmotic solutions (600 m-osmole/l) of sucrose, urea, NaCl and choline chloride. Pepsin output was stimulated maximally within 30 min and decreased thereafter, but remained at about 4--6-fold higher levels than during the previous irrigation with distilled water. Replacement of hyperosmotic instillates by distilled water reduced pepsin secretion to the initial level. Hypertonic ethanol (600 m-osmole/l) increased pepsin output only slightly. Vagotomy, pretreatment with atropine (1 mg/kg i.v.) or cimetidine (5 mg/kg i.v.), local anesthesia of the gastric mucosa with 4% lidocaine or intravenous infusion of PGE2 (2 microgram/kg X min) did not antagonise the stimulation of pepsin output induced by hyperosmotic NaCl (600 m-osmole/l). The results indicate that the increase of the osmolarity of intragastric instillates stimulates pepsin secretion in the rat without involvement of neural (vagal or local cholinergic reflexes) or hormonal mechanisms (release of gastrin) which are known to stimulate gastric secretion in the gastric phase.
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PMID:Osmotic stimulation of pepsin secretion in the rat. 35 99

Prostaglandins (PGs) participate in the inflammatory response, but the contribution of endogenously synthesized PGs to edema formation and increased vascular permeability is not known. Using a 10% scald burn in the rat, we measured water content (as percent, wet minus dry/wet weight) and 131I-RISA leakage (counts/g dry tissue) in scalded and normal skin at 30 minutes and 3 hr post injury. Four groups (10 rats/group) in each time period studied: control; scald; scald, 5 mg/kg indomethacin; scald, 10 mg/kg indomethacin. Indomethacin was administered intravenously 30 minutes before the scald; RISA was injected intravenously 30 min before termination of the study. In all indomethacin-treated groups immunoreactive plasma PGA was significantly lower (p less than 0.05) than in scalded, untreated groups. All scalded groups showed significantly higher RISA counts and water content than did the control group (p less than 0.01). At 30 min post-injury the indomethacin -treated groups did not differ from the untreated scald group (p greater than 0.20). In the 3 hour study all scalded groups had significantly higher content and RISA counts than control (p less than 0.01). Thus PGs produced during thermal trauma do not greatly contribute to the edema formation and increase in vascular permeability.
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PMID:Effect of inhibiting prostaglandin synthesis on edema formation and albumin leakage during thermal trauma in the rat. 50 95

In experiments in which blood was cross-circulating in rats, the blood pressure of the recipient dropped while that of the donor rose, following the increase of the circulating blood volume, produced by infusion either of saline or blood. The phenomenon was almost imperceptible when binephrectomized animals were used. In experiments in which the blood-bathed organ technique was used, prostaglandin-like substances were detected, released during the rise of the blood pressure, produced by the same stimulus (the expansion), in anaesthetized rats. A significant difference was found between the prostaglandin-like substances detected using the blood-bathed organ technique, in normal rats (5.387 ng per ml of blood plus or minus 0.288 = SEM) and those detected in binephrectomized rats (3.202 ng per ml of blood plus or minus 0.330, p smaller than 0.025). The biologically active substances detected in 25 ml of blood collected during expansion, while the assay organs showed a prostaglandin-like activity, were found to have the chromatographic behaviour and the bioassay properties of PGA, PGE and PGF series. A great quantity of the biologically active substances, having the chromatographic behaviour and the bioassay properties of PGA, PGS and PGF was detected in the rat renal medulla. Sufficient quantities of the released prostaglandin-like substances could escape the pulmonary vascular bed in this species of animal. It was concluded that a great quantity of the released prostaglandin-like substances came from the kidney and their release by this particular mechanism suggested that they play an important homeostatic role on the blood pressure, blood volume, and sodium and water balance regulation.
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PMID:[Origin, nature, role and fate of prostaglandins liberated during the expansion of intravascular space in the anesthetized rat]. 109 32

The renal prostaglandins PGS2 and PGE2 possess potent antihypertensive and vasodepressor activity. The mechanism of blood pressure lowering effect is through peripheral arteriolar dilation with a fall in total peripheral resistance. PGA unlike PGE escape degradation by the lung and thus could circulate as antihypertensive hormones. Since plasma PGA levels rise in humans on a low sodium intake, it has been postulated that the beneficial effects of a low sodium diet in some hypertensives may be the result of an increase in peripheral vasodilating PGA. Support that plasma PGA may be a regulator of systemic blood pressure is also derived from the fact a PGA-secreting renal tumor was associated with a fall in blood pressure and a rise in plasma PGA in a previously hypertensive woman. The removal of the tumor resulted in a return of blood pressure to elevated levels and a concomitant fall in PGA. Recently, a number of human patients with essential hypertension have been infused with PGA1 and PGA2. It was observed that there was an initial increase in renal blood flow, sodium and water excretion which was associated with no change in the elevated blood pressure. When blood pressure ultimately fell, there was a return of renal blood flow, sodium and water excretion to preinfusion levels. It would appear that PGA compounds act as 'ideal' antihypertensive agents since they favorably effect renal resistance, sodium and water homeostasis, plasma volume, total peripheral resistance, blood pressure and indirectly cardiac output through baroreceptor stimulation, all factors known to be important in etiology in human hypertension.
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PMID:Renal prostaglandins. 110 Oct 92

Prostaglandins PGE-1 or PGA-1 (0.5 to 1 mug per min) were infused into the stenosed renal artery of anesthetized hypertensive dogs. Increased urine volume, sodium and potassium excretion, and p-aminohippurate clearance were found during the prostaglandin infusion period in the infused kidney as compared to the control periods before infusion. Creatinine clearance was increased during infusion of PGE-1. The noninfused, nonischemic kidney showed no effect at the time of infusion with PGE-1 but in the case of PGA-1, the p-aminohippurate and creatinine clearances and urine diuresis were decreased. As a result, the mean aortic blood pressure decreased. Both prostaglandins increased the renal vein renin in the infused kidney. PGA-1 did affect renin release of the noninfused kidney, but PGE-1, which is rapidly inactivated by the lung, did not have this effect. Renin release seems to be influenced by electrolyte diuresis operating through the macula densa mechanism. However, the lowering of blood pressure seen in this study cannot exclude the involvement of the stretch receptors (the juxtaglomerular cells) for renin release. The increased renin release after prostaglandin administration seems to be a protective renal mechanism against the drug-induced hypotension. It seems to be induced by the direct sodium and water diuretic effects of prostaglandins.
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PMID:Direct effect of prostaglandins in renal function and renin release in the presence of renal ischemia in the dog. 111 61

A specific, sensitive and accurate radioimmunoassay (RIA) method for the measurement of prostaglandin A1 (PGA1) in either human whole blood or plasma is described. Whole blood is immediately lysed with distilled water containing tritiated indicator. When plasma is assayed, the blood samples are handled at 4 C and rapidly centrifuged. The lysate or plasma is adjusted to pH 5 with buffer and quickly extracted with 5% methanol in dichloromethane. The whole blood or plasma extract is then purified by Sephadex LH20 chromatography using the system methanol: methylene chloride (5:95) which separates the major groups of PGA, PGE and PGF. The RIA is then performed using an antiserum generated in rabbits from PGA1 coupled to bovine thyroglobulin. The antibody is highly specific, possessing very low cross reactivity to other prostaglandins (PGA2, PGE, PGB and PGF). Activated florisil or ammonium sulfate can be used to separate bound from free prostaglandin. This whole blood or plasma method yields blank values of only 2 +/- 2 pg per sample with a between assay precision determined by duplicate analysis of 8% and interassay precision of 3%. The mean whole blood PGA1 concentration in 27 subjects in 2.5 +/- 1.6 (SD) ng per 100 ml. No significant sex difference in PGA1 levels was noted and values were similar whether measured in whole blood or cooled plasma rapidly prepared and extracted. These values of PGA1 are much lower than those RIA values reported by others for "PGA" using antibodies with lower specificities.
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PMID:A radioimmunoassay for prostaglandin A1 in human peripheral blood. 115 43

Pepsin successfully catalyzed the synthesis of several peptide derivatives from N-protected di- or tripeptides and amino acid or peptide esters or p-nitroanilides in dimethylformamide-water solutions at pH 4.6. An optimal substrates:pepsin ratio depended on the structure of starting peptides, especially their fit to the substrate binding sites of the enzyme. For hexapeptide Z-Ala-Ala-Phe-Leu-Ala-Ala-OCH3 formation, an equilibrium yield was attained at 1:3.10(5) enzyme-substrates ratio that indicated high efficiency of pepsin in synthesis reactions. In the course of the equilibrium peptide synthesis, pepsin gradually disappeared from the liquid phase due to its entrapment within a gel, formed by the hexapeptide product, while retaining its activity. The inclusion into the precipitate was not specific for pepsin, so far as inert proteins, lysozyme, ribonuclease A and carbonic anhydrase, when added to the reaction mixture, became also co-precipitated with the hexapeptide formed. It appears that co-precipitation of pepsin, an important factor limiting the enzyme efficiency, might be operative as well for other proteinases used to catalyze peptide synthesis.
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PMID:Pepsin as a catalyst of peptide synthesis. Enzyme co-precipitation with emerging peptide products. 142 33

Pepsin was shown to catalyze synthesis of esters or p-nitroanilides tri-, tetra-, penta- and hexapeptides of general formula Z-X-Y-B, where X = Ala-Phe, Phe-Met, Ala-Ala-Glu, Ala-Ala-Phe, Ala-Ala-Leu, Ala-Ala-Trp, Ala-Ala-Met. Y = Ala, Leu, Val, Phe, Arg, Ala-Ala, Gly-Gly, Leu-Ala-Ala, Phe-Ala-Ala. B = OMe, pNA. The reactions were carried out in dimethylformamide-water solutions at pH 4.6 by equimolar ratio of amino- and carboxyl components (with the exception of Arg-pNA taken in 2-fold excess). The amount of pepsin in the reaction approached 1:1700 enzyme: substrate molar ratio although it might be improved--up to 1:3.10(5) for relatively long peptides.
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PMID:[Pepsin in the enzymatic synthesis of esters and n-nitroanilide peptides]. 144 35

Exchange-inert beta, gamma-bidentate Cr(H2O)x(NH3)y ATP complexes inactivate yeast phosphoglycerate kinase (PGK) by forming a coordination complex at the enzyme active site. The observed inactivation rates ranged from 0.019 min-1 to 0.118 min-1 for Cr(NH3)4ATP and Cr(H2O)4ATP, respectively. Incorporation of one mol of Cr-ATP to the enzyme was sufficient for complete inactivation of the enzyme. The presence of Mg-ATP protected the enzyme against inactivation by Cr-ATP. The other substrate 3-phosphoglycerate (3-PGA), when present, reduced the observed inactivation rates. The reduction of the k(obs) by 3-PGA was proportional to the number of NH3 ligands present in the coordination sphere of Cr3+ in the Cr-ATP complex, suggesting that in the ternary enzyme-Cr-ATP-3-PGA complex 3-PGA may be coordinated to the metal ion. When the effector sulfate ion was present, the presence of 3-PGA did not cause any further effects on the observed inactivation rates. This suggests that bound substrates are in a different arrangement at the active site when sulfate is present and therefore 3-PGA may not need to displace a ligand from Cr3+. Additionally, PGK exhibited a stereoselectivity for the binding of Cr(H2O)4ATP. delta diastereomer of Cr(H2O)4ATP yielded an order of magnitude smaller Ki value compared to the value observed with the lambda isomer. The recovery of enzyme activity was observed over a period of a few hours upon removal of excess Cr-ATP. The presence of substrates and/or effector ion sulfate did not alter the observed reactivation rate. There was no difference in the reactivation rates of the enzyme which was inactivated with Cr(H2O)4ATP or Cr(NH3)4ATP with and without 3-PGA. Increasing the ligand exchange rates of Cr3+ of Cr-ATP by increasing the pH value of the recovery medium from 5.9 to 6.8 increased the rate of recovery by a factor of 8. The pH dependence of the reactivation indicated that one hydroxyl group is involved in the recovery of the enzyme activity in enzyme CrATP and enzyme.CrATP.3-PGA complexes.
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PMID:Inactivation of yeast phosphoglycerate kinase by Cr-ATP complexes and its implications on the conformation of the enzyme active site. 144 68


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