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Query: UNIPROT:P00790 (PGA)
 2,475 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Three prostaglandins (PGE(2), PGF(2alpha) and PGA(2)) are present in rabbit kidney medulla. An acidic lipid extract (0.165g) obtained from 2kg of frozen rabbit kidney cortex was separated by silicic acid chromatography to yield eluates containing fatty acids, possible non-polar prostaglandin metabolites, PGA, PGE and PGF compounds. Ultraviolet spectra of the eluates before and after treatment with sodium hydroxide did not yield chromophores typical of any known prostaglandins or related metabolites. By using more sensitive bioassay procedures (contraction of rabbit duodenum) weak activity equivalent to 60mug of PGE(2) and 10mug of PGF(2alpha) was detected in the PGE and PGF eluates respectively. Extraction and bioassay of fresh kidney cortex revealed no prostaglandin-like activity. Attempts to biosynthesize prostaglandins in fresh homogenates of rabbit kidney cortex from endogenous precursors and from added arachidonic acid were unsuccessful. When freshly prepared homogenates of rabbit kidney cortex were incubated with added PGE(1) no evidence of enzymic breakdown was obtained. It is concluded that rabbit kidney prostaglandins are present predominantly in the medulla and there are no cortical mechanisms for their biosynthesis or inactivation under normal conditions.
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PMID:Distribution of prostaglandins in rabbit kidney. 543 88

1. Prostaglandins A(1), E(1), F(1alpha) and F(2alpha) were infused into the vertebral artery of the chloralose-anaesthetized greyhound and the resulting cardiovascular responses were compared with those obtained on intravenous and intracarotid infusions in the same dose range.2. Infusions of PGF(2alpha) intravertebrally (4-64 (ng/kg)/min) caused an increase of blood pressure, tachycardia and a fall of central venous pressure. Cardiac output was increased and peripheral resistance was essentially unchanged. There was never any response to intravenous or intracarotid PGF(2alpha) infusions in this dose range.3. PGF(1alpha) was found to have similar effects to PGF(2alpha) but it was much less potent.4. PGE(1) infusions (4-360 (ng/kg)/min) into the vertebral artery caused a tachycardia which was greater than that obtained with intracarotid or intravenous infusions, but there was no significant effect on blood pressure.5. Infusions of PGA(1) caused a small fall of blood pressure accompanied by an increase of heart rate and the dose response relationships were similar for all three routes of administration.6. It is concluded that some prostaglandins can activate cardioregulatory centres within the territory of distribution of the vertebral artery. Prostaglandin F(2alpha) is the most potent of these.
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PMID:Cardiovascular effects of prostaglandins mediated by the central nervous system of the dog. 547 2

Human lung explants maintained in culture for 7 d incorporate [(3)H]glucosamine into mucous glycoproteins. Ethanol-precipitable, glucosamine-labeled mucous secretion was measured, and the effects of different pharmacologic agents upon this secretion were investigated. Anaphylaxed human lung generates prostaglandin (PG) synthesis and increased mucous release. Arachidonic acid (AA), PGA(2), PGD(2), and PGF(2alpha) significantly increased mucous glycoprotein release, whereas PGE(2) significantly reduced release. Evidence which suggests that lipoxygenase products of AA augment mucous release includes the following: (a) Nonsteroidal anti-inflammatory drugs (NSAID: acetylsalicylic acid and indomethacin) increase mucous release while preventing prostaglandin formation. (b) The increase in mucous release induced by AA or NSAID is additive once the agents are combined. (c) Several nonspecific lipoxygenase inhibitors (eicosa-5,8,11,14-tetraynoic acid; vitamin E; nordihydroguaiaretic acid; and alpha-naphthol) inhibit mucous release. Three additional lines of evidence directly indicate that monohydroxyeicosatetraenoic acid (HETE) causes increased mucous release: (a) the addition of a mixture of synthetic HETE (24-600 nM) increases mucous release; (b) pure 12-HETE (1-100 nM) also increases mucous release; (c) mucous release is increased synergistically by the combination of HETE and NSIAD. These data taken together demonstrate that HETE are capable of increasing mucous release and that conditions which may influence HETE production alter mucous release. Thus, although not directly demonstrating HETE production by human airways, the data strongly suggest that lipoxygenase products of AA in airways may profoundly influence mucous release; and it seems possible that lipoxygenase inhibitors may have a role in treating bronchorrhea.
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PMID:Effects of arachidonic acid, monohydroxyeicosatetraenoic acid and prostaglandins on the release of mucous glycoproteins from human airways in vitro. 678 82

Effects of the administration of PGs A-1, E-2 and F-2 alpha (150 micrograms/rat b.i.d. for 10 days) were studied. Significant increase in testicular weight was observed only in PGE-2 treated group. Testicular ascorbic acid content reduced significantly by treatment with all the PGs. PGE-2 treatment caused a significant decrease in the content of testicular cholesterol, while no change was observed in the same and prostatic acid phosphatase activity in any of the PG treated groups. Blood plasma levels of testosterone drastically reduced by both PGE-2 and PGF-2 alpha, while there was no change in the levels of plasma LH in any of the groups. Plasma FSH levels increased significantly in PGA-1 treated rats only. The results suggest that 1) There is a direct action of PG particularly PGE-2 on testicular weight. PGE-2 increases testicular weight possibly by preventing degeneration of spermatids, 2) PGE-2 acting directly on the testis, reduces testicular ascorbic acid content, stimulates the conversion of cholesterol to pregnenolone but depresses the conversion of the latter to testosterone.
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PMID:Effect of prostaglandins A-1, E-2 and F-2 alpha on blood plasma levels of testosterone, LH and FSH in male rats. 678 15

1. The effect of i.v. administration of prostaglandin (PG) E(2) (10-40 mug kg(-1) h(-1)), 16,16-dimethyl PGE(2) (0.1-0.5 mug kg(-1) h(-1)), PGE(1) (16-20 mug kg(-1) h(-1)), PGA(1) (5-11 mug kg(-1) h(-1)) and PGF(2alpha) (40 mug kg(-1) h(-1)) on the relationship between [H(+)] and flow of gastric juice during stimulation of gastric secretion by pentagastrin was investigated in conscious cats prepared with cannulated gastric fistulae.2. A- and E-type prostaglandins significantly reduced pentagastrin-stimulated acid output. This inhibition was associated with a reduction of the [H(+)] of the gastric juice such that the [H(+)] observed at any flow rate tended to be lower than the normal range observed with pentagastrin alone. With the highest doses of these prostaglandins the mean [H(+)] values were well below the normal range with pentagastrin alone.3. At the dose tested, PGF(2alpha) had little effect on acid output, and did not alter the relationship between [H(+)] and gastric flow.4. There is a linear relationship between acid output and gastric flow and this relationship is similar during stimulation of gastric secretion by pentagastrin, histamine or insulin. Gastric acid inhibitory doses of cimetidine, atropine and somatostatin did not alter this relationship. In contrast the A- and E-type prostaglandins displaced this relationship to the right of the normal line observed with the acid stimulants alone. A- and E-type prostaglandins reduced the slope of the line relating acid output and gastric flow from approximately 150-170 muequiv/ml(-1) to approximately 100-120 muequiv ml(-1), this being taken as evidence of dilution of the parietal H(+) secretion with a non-parietal secretion.5. The volume of non-parietal gastric secretion was calculated as the gastric flow at zero acid output by extrapolation of linear plots of acid output versus gastric flow. Unstimulated gastric flow measured directly was 0.75 ml 15 min(-1). The calculated non-parietal flow was in the range 0.52-0.90 ml 15 min(-1) during stimulation of gastric secretion with pentagastrin, histamine and insulin, and inhibition of pentagastrin-stimulated acid secretion with cimetidine, atropine and somatostatin. PGE(2) (1.51 ml 15 min(-1)) and 16,16-dimethyl PGE(2) (1.20 ml 15 min(-1)) nearly doubled the calculated non-parietal flow.6. These data demonstrate that gastric acid inhibitory doses of A- and E-type prostaglandins can reduce the [H(+)] in the bulk fluid of the gastric lumen during stimulation of acid secretion. The data provide evidence that these prostaglandins stimulate a non-parietal component of gastric secretion. This might be gastric bicarbonate and mucus secretion.
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PMID:Prostaglandins alter the relationship between gastric hydrogen ion concentration and flow: evidence for stimulation of non-parietal secretion in the cat. 694 8

Three cows and 2 sheep were passively immunized against prostaglandin (PG) F on Day 16 and Days 13-15 of the oestrous cycle respectively. The PGF antiplasma was raised in ovariectomized ewes against a PGF-2 alpha-bovine serum albumin complex and showed 100%, 12.5%, 0.3%, less than 0.05% and less than 0.01% cross-reactivity with PGF-2 alpha, PGE-2, PGA-2, PGB-2 and arachidonic acid, respectively. Control animals were given an equivalent amount of ovariectomized ewe plasma. In all passively immunized animals there was evidence of a persistent corpus luteum as indicated by plasma progesterone concentration and the failure of the animals to return to oestrus until at least 29 days after treatment. These data are consistent with previous proposals that PGF-2 alpha is the uterine luteolytic factor in sheep and cattle.
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PMID:Prolongation of the oestrous cycle in cows and ewes after passive immunization with PGF antibodies. 719 12

1 The sensitivity and contractility of isolated canine intrapulmonary arteries and veins to a variety of primary prostaglandin compounds was studied.2 Intrapulmonary arteries produced no measurable contractile responses to prostaglandin A(1) (PGA(1)), PGA(2), PGB(1), PGD(2), PGE(1), PGE(2) or to PGF(1alpha). However, high concentrations of both PGB(2) (> 10(-7) M) and PGF(2alpha) (> 10(-6) M) elicited concentrated-related, but weak, contractile responses, measuring only 5-25% of KCl-induced maximum contractions.3 Intrapulmonary arteries, partially contracted by 5-hydroxytryptamine (5-HT), exhibited concentration-related relaxations in response to PGE(1); PGE(2), PGA(1) or PGA(2) produced only weak superimposed contractions.4 In contrast to intrapulmonary arteries, intrapulmonary veins contracted in a concentration-related fashion to all prostaglandins tested, where the contractile sensitivity was (based on EC(50) s and threshold concentrations): PGB(2) > PGB(1) > PGD(2) > PGF(2alpha) > PGA(2) >> PGA(1) > PGF(1alpha) > PGE(2) > PGE(1).5 In terms of the ability to generate maximum contractile responses on intrapulmonary veins, the prostaglandins were also variable, with PGA(2) and PGB(2) being the most potent and PGD(2) the least potent.6 Intrapulmonary veins, partially contracted by 5-HT, exhibited concentration-related relaxations to PGE(1) at low concentrations, followed by secondary contractile responses at higher concentrations.7 Neither PGA(1) nor PGA(2) (3.4 x 10(-8) to 3.4 x 10(-5) M) inhibited or potentiated 5-HT responses of intrapulmonary arteries.8 These data suggest that there are species, regional and major qualitative and quantitative, differences in the responsiveness of intrapulmonary arteries and veins to prostaglandin.
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PMID:Differential effects of prostaglandins on canine intrapulmonary arteries and veins. 727 85

Rats were treated with twice daily injections of 100 microgram PG/rat for 15 days. PGA-1 had no effect. PGE-2 caused a significant increase in testicular weight, RNA content, hyaluronidase activity and number of spermatids. PGF-2 alpha produced a significant decrease in sorbitol dehydrogenase activity and DNA content. It is suggested that PGE-2 may be involved in later stages of spermatogenesis, i.e. conversion of spermatocytes to spermatids.
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PMID:Effect of prostaglandins A-1, E-2 and F-2 alpha on spermatogenesis in rats. 735 86

We describe prostaglandin (PG) biosynthesis by microsomal-enriched fractions of fat body prepared from true armyworms, Pseudaletia unipuncta. PG biosynthesis was sensitive to experimental conditions, including incubation time, temperature, pH, substrate and protein concentration. Optimal PG biosynthesis conditions included 1 mg of microsomal-enriched protein, incubated at 28 degrees C for 7.5 min at pH 8. These preparations yielded four major PGs: PGA(2), PGE(2), PGD(2) and PGF(2alpha). PGA(2) and PGE(2) were the predominant eicosanoids produced under these conditions. Two non-steroidal anti-inflammatory drugs, indomethacin and naproxen, effectively inhibited PG biosynthesis. Unlike other invertebrate PG biosynthetic systems studied so far, the true armyworm system appeared to be independent of the usual exogenous co-factors required by mammalian and other invertebrate systems. These findings are discussed with respect to PG biosynthesis in other invertebrate and vertebrate systems.
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PMID:Prostaglandin biosynthesis by fat body from true armyworms, Pseudaletia unipuncta. 1122 53

The role of transforming growth factor alpha (TGFalpha) and prostaglandins (PGs) in the preferential growth of preneoplastic liver cells was studied. Rats received the genotoxic hepatocarcinogen N-nitrosomorpholine (NNM); placental glutathione S-transferase (GSTp) was used as a marker to identify preneoplastic foci. Preneoplastic foci expressing TGFalpha (TGFalpha(+)) grew more rapidly than TGFalpha negative (TGFalpha(-)) ones. Almost all tumours studied were positive for TGFalpha. The key enzymes of prostaglandin synthesis, cyclooxygenase I (Cox-1) and II (Cox-2), were present in all unaltered and preneoplastic cells and tended to decrease in the later stages of hepatocarcinogenesis. Immunostaining revealed that cultures of hepatocytes, isolated from NNM-treated livers by collagenase perfusion, contained 1-2% GSTp-positive (GSTp(+)) and 9% TGFalpha(+) hepatocytes; 0.6% of the cells were GSTp(+)/TGFalpha(+). Cox-1 and Cox-2 were present in all cells. DNA replication was almost exclusively associated with expression of TGFalpha. GSTp(+) hepatocytes showed a 3- to 4-fold higher probability of TGFalpha expression and of DNA synthesis than GSTp-negative (GSTp(-)) cells. PGE(2) or PGF(2alpha) increased expression of TGFalpha and DNA replication in GSTp(-) cells but not in GSTp(+) cells. PGA(2) and PGJ(2) decreased DNA synthesis in TGFalpha(+) cells without an obvious effect on the intracellular levels of TGFalpha. The Cox-2 inhibitor SC236 suppressed DNA replication preferentially in GSTp(+) cells; this inhibition was reversed by PGE(2)/F(2alpha). Indomethacin had no effect. These results suggest the following conclusions. (i) Growth regulation of preneoplastic GSTp(+) cells in culture exhibits distinct differences from GSTp(-) cells and elevated expression of TGFalpha contributes to their growth advantage. (ii) TGFalpha renders preneoplastic hepatocytes sensitive to suppression of DNA synthesis by PGA(2)/J(2). (iii) SC236, a Cox-2 inhibitor, may have preventive value in hepatocarcinogenesis.
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PMID:Role of transforming growth factor alpha and prostaglandins in preferential growth of preneoplastic rat hepatocytes. 1147 Jul 56


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