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At least 19 recordsLinked to original sources
PubMed1976

The content of prostaglandin E and prostaglandin F2alpha in the exudate of carrageenin granuloma of rats.

1. Granuloma was made by the subcutaneous injection of 2% carrageenin solution on the dorsum of male rats. Eight, 16, 24 and 72 h after the injection. the exudate from each rat granuloma was withdrawn and extracted for rpstaglandins. 2. Extracted prostaglandins were separated prostaglandin E and prostaglandin F group by silicic acid mini-column chromatography. Then the amount of prostaglandin E and prostaglandin F2alpha were determined by the radioimmunoassay method. 3. The levels of prostaglandin E in the granuloma exudates were 4.6 ng/ml at 8 h after the carrageenin injection, then decreased 3.6 ng/ml and to 1.1 ng/ml at 16 h and 24 h, respectively. Seventy-two h after the injection, prostaglandin E level was increased to 8.1 ng/ml. 4. The levels of prostaglandin F2alpha in the exudate were as follows: At 8 h after the carrageenin injection, the level was 9.4 ng/ml, then decreased to 1.3 ng/ml and to 0.8 ng/ml at 16 h and 24 h, respectively. Seventy-two h after the carrageenin injection, it was again elevated to 4.7 ng/ml. 5. The exudate of granuloma, 24 and 72 h after the carrageenin injection, was incubated with [3H]prostaglandin E1 at 37 degrees C for 30 min. Then the acidic ether extract was subjected to reversed phase partition chromatography. It was found that the exudate of 24 h and 72 h granuloma had little activity of prostaglandin 15alpha-hydroxy dehydrogenase.

Animals↗
PubMed1977

A technique for the immunohistochemical localization of prostaglandin E.

Prostaglandin E (PGE) has been localized via the unlabeled antibody technique in freeze-dried and ethanol-fixed cryostat sections. Discrete perivascular and stromal localization was present in the uterus prepared by the method presented, but not in classically fixed specimens. Absorption of the anti-PGE by addition of free PGE was ineffective; whereas, removal of PGE-reactive antibodies from the anti-serum was effectively accomplished with an Affigel-101-PGE immunoadsorbant column.

Animals↗
PubMed1976

Quantifications of the major urinary metabolite of the E prostaglandins by mass spectrometry: evaluation of the method's application to clinical studies.

Measurement of 7alpha-hydroxy-5,11-diketotetranoprostane-1,16-dioic acid, (PGE-M), the major urinary metabolite of prostaglandin E1 and E2 in man provides a useful indicator to monitor prostaglandin biosynthesis. For quantitative analysis of this prostaglandin metabolite and the stable-isotope dilution techniqe of selected ion monitoring (SIM) is employed using gas-liquid chromatography-mass spectrometry. The preparation of the bis(D3-methyloxime), bis-methyl ester of PGE-M containing a tritium tracer in position 2 which was used as internal standard for the SIM method is described. The synthesis of this internal standard includes the biosynthetic conversion of 11-hydroxy-9,15-diketoprostanoic acid to PGE-M by the rabbit. The intra-assay coefficient of variation of this SIM method ranged between 4.0 to 6.7 percent. The recovery of authentic, underivatized PGE-M added to urine was 93 +/- 3% (mean +/- SEM, n=17). The levels of PGE-M excreted in urine were higher (p less than 0.001) in males than in females (15.2 +/- 1.9 mug/24 hours (n=24) and 3.3 +/- 0.3 mug/24 hours (n=17), respectively. These levels were in close agreement with values published previously. No significant difference in excretion of PGE-M between the sexes was observed in the pre-pubertal age-grou (male: 2.9 +/- 0.8 mug/24 hours, n=5; female: 3.1 +/- 0.9 mug/24 hours, n=5) or in the age-group of 45-80 years (male: 9.3 +/- 1.1 mug/24 hours, n=21; female: 7.3 +/- 0.9 mug/24 hours, n=12). The amount of PGE-M excreted decreased significantly after administration of indomethacin or acetyl salicylic acid in therapeutic doses. The concomitant reduction of the urinary excretion of PGE-M (68 to 85% decrease) and prostaglandin E (73 to 100% decrease) after indomethacin treatment in each case (n=8) is evidence that a diminished urinary PGE-M output reflects a decrease in prostaglandin E biosynthesis.

Adolescent↗
PubMed1975

Purification and regulatory properties of chicken heart prostaglandin E 9-ketoreductase.

Prostaglandin E 9-ketoreductase was purified from chicken heart by ammonium sulfate fractionation, and DEAE-Sephadex, hydroxylapatite and phosphocellulose chromatography. Two peaks of activity were resolved during the phosphocellulose chromatographic step. Both peaks were stimulated by a substance that was not bound to the phosphocellulose column. This stimulatory substance was destroyed by treatment with phosphodiesterase and 0.1 M NaOH. It was heat-stable (100 degrees, 2 min), nondialyzable, and resistant to treatment with pronase, ribonuclease, and deoxyribonuclease; but it was dialyzable after heating or digestion with pronase. Sodium pyrophosphate also enhanced the activities of the prostaglandin E 9-ketoreductases as did angiotensin I; but not angiotensin II. In the presence of 3':5'-cyclic AMP, AMP, or several other ribonucleotides, the enhancing effects of the natural stimulatory substance, sodium pyrophosphate or angiotensin I were blocked, but these ribonucleotides themselves had little effect on the enzymes activity. The substrate specificities of the two prostaglandin E 9-ketoreductases were also studied. Both the 9-keto group and the 15-keto group of 15-ketoprostaglandin F2 alpha could be converted to the corresponding hydroxyl group; the 15-keto group was reduced faster than the 9-keto group. Prostaglandin D2, a prostaglandin with a 9-hydroxyl and an 11-keto group, could not be converted to prostaglandin F2 alpha nor could cyclohexanone be converted to cyclohexanol by the prostaglandin E 9-ketoreductase.

Alcohol Oxidoreductases↗
PubMed1979

Variability in rates of urine prostaglandin E excretion.

Urine prostaglandin E excretion rates were determined by hepatic receptor assay in three groups of conscious animals. Although 24-hour urine collections gave reproducibly similar levels of prostaglandin E excretion rates, levels obtained with consecutive 20-minute urine collections were extremely variable despite no obvious changes in renal function. Since short urine collection periods are used frequently in physiologic studies, the significance of variations in prostaglandin excretion rates in these studies may have to be re-evaluated.

Animals↗
PubMed1976

Peripheral plasma determinations of prostaglandin E in asthmatics.

Prostaglandins, unsaturated fatty acid derivatives with diversified pharmacologic activity, have recently been implicated in the pathophysiology of reversible airway disease. This study attempted to elucidate baseline prostaglandin E (PGE) plasma levels in asthmatics and the change in these levels after stimulation by a beta-adrenergic agent. Fourteen stable, ambulant patients with reversible airway disease and 28 nonatopic control subjects were studied. All had baseline PGE levels performed. The asthmatics were asked to abstain from all medication for 10 hr prior to evaluation. After baseline evaluation consisting of plasma PGE determination, pulmonary function test, blood pressure, and heart rate, 375 mug of aerosolized terbutaline sulfate was administered to 8 of the asthmatics plus 4 of the nonatopic control subjects; the above measurements were repeated at 15, 30, and 60 min after administration. There was a statistically significant difference in baseline plasma PGE levels between the asthmatics (PGE = 432 +/- 81) and the nonatopic control subjects (PGE = 89 +/- 9) (p less than 0.002). Following terbutaline administration, there was no significant change observed in PGE levels in asthmatic or in control individuals (asthmatics: 0 min, 570, 15 min, 513, 30 min, 514, 60 min, 608; normal subjects: 0 min, 138, 15 min, 137, 30 min, 143, 60 min, 214). In summary, we observed a significant difference in baseline PGE levels between asthmatic and nonatopic control persons. No change, however, was noted in PGE levels after beta-adrenergic receptor stimulation. This observation is consistent with the current hypothesis that beta-adrenergic agents act independently of prostaglandins to increase adenyl cyclase and modify bronchiole smooth muscle tone.

Adult↗
PubMed1979

Zero extracellular K+ and prostaglandin E release in the guinea-pig taenia coli.

Prostaglandin E release rates from isolated strips of guinea-pig taenia coli increased during exposure to zero K+ bathing fluid, from control values of 0.78 +/- 0.11 ng/g per min to levels as high as 29.2 ng/per min. Release rates increased for 40-50 min and then remained constant or fell despite progressive increases in intracellular sodium [Nai+] or fall in intracellular potassium [Ki+]. Readmittance of K+ to the bathing solution resulted in rapid reversal of elevated prostaglandin E release rates. [Nai+] and [Ki+] were markedly more abnormal in strips exposed to zero K+ for 70-201 min compared to 30-min exposures. Upon the readdition of K+ after long zero K+ exposure, the rate of prostaglandin E release fell long before [Nai+] and [Ki+] returned to control levels. After K+ was readded to the bathing solution, the ion concentration of tissues exposed to zero K+ for 30 min returned to normal much more quickly than did those of tissues exposed for the longer time periods, yet the exponential rate constants for fall of prostaglandin E release rate after K+ was added were not significantly different after short or long zero K+ exposure. Thus there was a dissociation between the return of [Nai+] and [Ki+] and the fall of prostaglandin E release rate to control levels. Ouabain augmented prostaglandin E release under conditions where [Ki+] could not fall. Addition of known neurotransmitters present in this tissue to the bathing fluid did not augment prostaglandin E release. Guinea-pig taenia coli strips that had been incubated with [3H]arachidonic acid, constantly released [3H]arachidonic acid and [3H]prostaglandin E and a prostaglandin which cochromatographed with prostaglandin E but could not be converted to prostaglandin B by alkali and was shown to be 6-ketoprostaglandin F1 alpha. Release of [3H]arachidonic acid and [3H]prostaglandin E plus 6-[3H]ketoprostaglandin F1 alpha was increased when strips were exposed to zero K+. Data obtained in this study suggest the augmented prostaglandin E release seen during zero K+ or ouabain is related to increased availability of unbound arachidonic acid at the site of cyclooxygenase in the cell. Augmented prostaglandin E release is apparently not related to alterations in intracellular electrolyte concentrations or release of known neurotransmitters.

Acetylcholine↗
PubMed1977

Prostaglandins E and F in uterine venous plasma in relation to peripheral plasma levels of progesterone and 20alpha-hydroxyprogesterone in the rat throughout pregnancy and parturition.

Prostaglandins E and F in uterine venous plasma and progesterone (P) and 20alpha-hydroxyprogesterone (20alpha-OH-P) in peripheral plasma were measured by radioimmunoassays throughout pregnancy and parturition in the rat. E Prostaglandins are low (approx. 2 ng/ml) and maintain a more or less constant level throughout most of the pregnancy except just before parturition when they rise to 3.8 ng/ml on day 20. F Prostaglandin levels are always higher than E prostaglandins and show distinct peaks around day 5 (5 ng/ml), day 11 (7 ng/ml), and before parturition (8.4 ng/ml). Progesterone levels are higher than 20alpha-OH-P levels throughout most of the pregnancy (day 6-20); however, during early pregnancy (day 1-5) and before parturition more 20alpha-OH-P than P is present in peripheral blood. The possible role of uterine venous prostaglandin levels in altering the 20alpha-OH-P/P ratio during pregnancy and parturition is discussed.

Animals↗
PubMed1979

Prostaglandin E, thromboxane B2 and 6-oxo-prostaglandin F1 alpha in amniotic fluid and maternal plasma of rhesus monkeys (Macaca mulatta) during the latter third of gestation.

The concentrations of prostaglandin E (PGE), thromboxane B2 (TXB2) and 6-oxo-prostaglandin F1 alpha (6-oxo-PGF1 alpha) were measured by radioimmunoassay in serial samples of amniotic fluid and maternal peripheral plasma in the latter third of pregnancy in rhesus monkeys (Macaca mulatta). The samples were collected under ketamine-induced anaesthesia. The concentration of PGE was undetectable in amniotic fluid until a few days before delivery when a large increase was observed in three of the five animals. There were small increases of TXB2 and 6-oxo-PGF1 alpha in amniotic fluid before delivery. In maternal plasma the concentrations of PGE, TXB2 and 6-oxo-PGF1 alpha were generally higher and more variable than in amniotic fluid and did not increase with advancing gestation. It is suggested that increased production of primary prostaglandins occurs before, and is involved in, the onset of parturition in the rhesus monkey.

Amniotic Fluid↗
PubMed1979

Effect of triamterene on urinary excretion of immunoreactive prostaglandin E in essential hypertension.

The effect of triamterene on urinary excretion of prostaglandin E was studied, and the results were compared with those obtained with spironolactone. Urinary excretion of immunoreactive prostaglandin E was measured radioimmunologically. Triamterene was administered in a dose of 100 mg/day for 8 days to 7 patients with essential hypertension. Following the administration of triamterene, urinary prostaglandin E tended to increase. However, the increment was not significant. The lack of significant increase in urinary prostaglandin E excretion during the administration of triamterene contrasted with our previous finding with spironolactone, in which a significant increase in prostaglandin E excretion was observed on the first day of spironolactone administration. Urinary Na excretion and urinary Na/K ratio were significantly increased and urine volume also tended to increase following the administration of triamterene. Plasma renin activity and plasma aldosterone concentration were increased in all cases. However, there was no significant correlation between these parameters and urinary prostaglandin E. These results suggest that the effect of triamterene on renal prostaglandin E synthesis is different from that of spironolactone and that the change in urinary prostaglandin E after the administration of triamterene is not the reflection of the change in the renin-angiotensin-aldosterone system.

Adolescent↗
PubMed1978

Effect of spironolactone on urinary excretion of immunoreactive prostaglandin E in essential hypertension and primary aldosteronism.

To determine the effect of aldosterone antagonist on renal prostaglandin E synthesis, the rate of urinary excretion of immunoreactive prostaglandin E was measured radioimmunologically before and during the oral administration of an aldosterone antagonist, spironolactone, in 5 patients with essential hypertension, 3 with primary aldosteronism and 2 with postoperative primary aldosteronism. Spironolactone was administered at an oral dose of 25 mg 4 times daily for about 1 week. In the control state, the rates of urinary prostaglandin E excretion ranged from 151 ng/day to 4,527 ng/day in essential hypertension. The rates were not augmented in primary aldosteronism but decreased after the removal of an aldosterone producing adenoma. No obvious relationship was observed between plasma aldosterone concentration and the rate of urinary prostaglandin E excretion. On the first day of spironolactone administration, the excretion rates of urinary prostaglandin E were markedly increased independently of basal plasma aldosterone level in all cases except one case of essential hypertension. Urinary prostaglandin E excretion was increased with the concominant increase of urinary Na/K ratio in essential hypertension and primary aldosteronism. After the second day, the augmented urinary prostaglandin E excretion was decreased and the changes of urinary prostaglandin E excretion varied from case to case. These results suggest that synthesis of renal prostaglandin E is not mainly regulated by aldosterone in essential hypertension and primary aldosteronism.

Adult↗
PubMed1979

The concentrations of the prostaglandins E and F, 13 14-dihydro-15-oxo-prostaglandin F and thromboxane B2. In tissues obtained from women with and without pre-eclampsia.

The concentrations of prostaglandins E (PGE) and F (PGF), 13, 14-dihydro-15-oxo-prostaglandin F (PGFM) and thromboxane B2 (TXB2) were measured by specific radioimmunoassays in tissues obtained from women with and without pre-eclampsia. The concentrations of PGE in the amnion, chorion, decidua and placenta obtained from subjects with pre-eclampsia were significantly lower than those from subjects without pre-eclampsia. The concentration of PGE in these tissues increased significantly with gestational age and correlated with urinary oestrogen excretion. PGF concentrations were lower in the amnion and placenta of the pre-eclamptics compared to those without pre-eclampsia. The concentrations of PGFM in the amnion, decidua, and myometrium were lower in the pre-eclamptics. No significant difference in the TXB2 concentrations between the two groups of subjects were found. It is suggested that the altered tissue concentrations of prostaglandins in pre-eclamptics are due to the effects of gestational age and oestrogens and may or may not be involved in the pathogenesis of pre-eclampsia.

Adolescent↗
PubMed1979

[Development of estradiol, progesterone, and prostaglandins E and F2 alpha levels during pregnancy in mice].

17 beta estradiol, progesterone, prostaglandin E and prostaglandin F2 alpha were determined in the plasma of mice at different times of pregnancy. Estradiol displays a preimplantation peak on day 4. Other peaks are visible at the end of the implantation period (day 6) and on day 10. Progesterone increases when implantation begins (day 5). Prostaglandins increase at the beginning of pregnancy and decrease temporarily before implantation. Other peaks are also apparent for prostaglandin E on days 5.5 and 11.

Animals↗
PubMed1978

Stimulation of anterior pituitary prostaglandin E content and somatotropin (growth hormone) synthesis by phospholipase A.

The prostaglandin E content of dispersed rat anterior pituitary glands was found to increase in the presence of phospholipase A or arachidonic acid. The increases were abolished by the addition of indomethacin. Similarly, the rate of somatotropin (growth hormone) synthesis was increased by these two agents, and the increases were again abolished by indomethacin. Phospholipase A also stimulated somatotropin release. The stimulation of prostaglandin E accumulation was a specific response to those fatty acids that are precursors for prostaglandin synthesis. One such precursor, [3H]arachidonic acid, was incorporated by rat anterior pituitary glands in vitro, and found to be associated mainly with phosphatidylethanolamine-like material. It is concluded that the intracellular concentration of prostaglandin E is limited by the availability of precursor fatty acids and that this can be increased by the addition of exogenous precursors or by the action of exogenous phospholipase A on the cellular phospholipid. Factors that increased prostaglandin E concentrations also increase the rate of synthesis of somatotropin, providing further evidence for the concept that prostaglandin E is involved in modulation of the rate of synthesis of this hormone.

Animals↗
PubMed1978

Implication of renal prostaglandin E in urinary sodium excretion.

To investigate the role of renal prostaglandin in the regulation of sodium metabolism, ruinary prostaglandin E excretion, an indicator of renal prostaglandin synthesis, urinary sodium excretion, plasma renin activity and urinary aldosterone excretion were measured in 84 normal subjects and 55 patients with essential hypertension on ad lib intake of sodium. The excretion rates of urinary prostaglandin E were 736.8 +/- 32.2 ng/day in normal subjects and 394.3 +/- 28.7 ng/day in essential hypertensives. The excretion rate was significantly decreased in essential hypertensives (P less than 0.001). A significant positive correlation was found between urinary sodium excretion and urinary prostaglandin E excretion in normal subjects (r = 0.39, P less than 0.001), and in essential hypertensives (r = 0.62, P less than 0.001). There was no correlation between the renin-angiotensin-aldosterone system and urinary prostaglandin E excretion in normal subjects as well as in essential hypertensives. The present data show that renal prostaglandin might be involved in the renal handling of sodium, and prove the possibility that the decrease of renal prostaglandin synthesis is one of the etiological factors in essential hypertension.

Adolescent↗