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At least 127 records · Page 7Linked to original sources
PubMed1986

Specificity of PGE2 analogs interaction between food intake and antisecretory effect.

We evaluated the degree of acid suppression that occurred when enprostil, a dehydro-prostaglandin E2 (PGE2) methyl ester analog, was administered before (anti-cibum AC) or after a meal (post-cibum PC). A double-blind, randomized, single-dose, parallel-group design compared enprostil, 35 mcg, 25 min AC or 5 min PC, with placebo AC or PC in 30 healthy adults. Enprostil or placebo was administered at time 0 and a standard beef test meal was ingested at 25 min, followed 5 min later by enprostil or placebo. A second test meal was consumed at 210 min. Intragastric titration was performed from 30 to 390 min. Subjects receiving enprostil-AC or enprostil-PC secreted less (P less than 0.05) acid compared to placebo; however, the antisecretory effects of enprostil-AC or enprostil-PC were similar throughout the duration of study. Minor adverse reactions were present in 13/30 subjects and confined to those receiving enprostil. In contrast to the previously reported potentiation of trimoprostil, a trimethyl-desoxy-PGE2 analog, antisecretory activity by food, enprostil-PC did not result in more prominent or prolonged suppression of gastric acid secretion than enprostil-AC. There is an apparent specificity of different oral PGE2 analogs with regard to their antisecretory activity in the presence or absence of food.

Adult↗
PubMed1995

Receptor subtypes involved in dual effects induced by prostaglandin E2 in circular smooth muscle from dog colon.

Smooth muscle strips and isolated muscle cells from the circular layer of dog colon, were used to study the effect of prostaglandin E2 (PGE2) and their analogs acting at EP receptors: Iloprost (IP/EP1), butaprost (EP2) and enprostil (EP3) and SC19220 (antagonist EP1) to characterize the EP-receptors involved in the control of muscle function. In strips treated with tetrodotoxin, only enprostil provoked a concentration-dependent contraction. The concentration of enprostil inducing a half maximal contraction (EC50) was 400 nM and the maximal effect was obtained at 1 microM. PGE2, butaprost and iloprost induced a dose-dependent relaxation, with an EC50 of 200, 80 and 200 nM, respectively. The maximal relaxation was obtained at 1 microM for all these agents. When the EP1 antagonist, SC19220 (10 microM), was added 20 min before PGE2 or their analogs, their respective concentration-response curves were not affected. In isolated cells, PGE2 and enprostil induced a cell contraction in a concentration-dependent manner, whereas iloprost and butaprost had no effect by themselves. The maximal contraction was 241.1 +/- 1.7% at 10 nM PGE2 and 22.5 +/- 1.6% at 10 nM enprostil. EC50 of PGE2 and enprostil was 40 pM. SC 19220, at concentrations ranging from 1 pM to 0.1 microM, failed to inhibit the contraction induced by either PGE2 or enprostil. When cells were preincubated for 1 min with butaprost or iloprost at concentrations ranging from 1 pM to 1 microM, the contraction induced by CCK8 (10nM) was inhibited in a concentration-dependent matter.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Separation of the stereoisomers of an allenic E-type prostaglandin.

Enprostil (I) is a synthetic dehydro-prostaglandin E2 containing a chiral allene moiety which is unresolved relative to the four remaining chiral centers. The relative configuration of the four remaining chiral centers is consistent with that of the naturally occurring E series of prostaglandins. Thus, enprostil exists as enantiomeric pairs of two allenic epimers. An analytical procedure has been developed that separates the four optical isomers present in enprostil. This procedure involves, first, the acid-catalyzed dehydration of enprostil to its corresponding prostaglandin A analogue followed by derivatization with beta-naphthylsulfonyl-L-prolyl chloride. The resulting diastereomeric sulfonate esters are separated on an achiral silica gel high-performance liquid chromatographic column. This procedure has been applied to the analysis of both enprostil drug substance and enprostil formulated in a propylene carbonate solution from soft elastic gelatin capsules. An efficient procedure for the recovery of enprostil from the solution formulation is also described.

Chromatography, High Pressure Liquid↗
PubMed1986

Prostanoid inhibition of canine parietal cells.

Cellular mechanisms underlying the anti-secretory actions of the prostaglandin E2 analogue enprostil were studied using enzyme-dispersed, elutriator-enriched canine parietal cells and the accumulation of the weak base 14C-labeled aminopyrine as a functional index. Enprostil inhibited the accumulation of aminopyrine stimulated by histamine and the phosphodiesterase inhibitor isobutylmethyl, but not by carbachol, gastrin, or dibutyryl cyclic adenosine monophosphate. Inhibition by enprostil was dose-dependent (0.1 nM to 1 microM), with maximal inhibition ranging from 65 to 95 percent. Over the same concentration range, enprostil inhibited the histamine-stimulated generation of cyclic adenosine monophosphate. This selective inhibition of histamine activation of parietal cell function was comparable to that found for prostaglandin E2. Forskolin, a diterpene that directly activates the catalytic subunit of adenylate cyclase, was also markedly inhibited by nanomolar concentrations of prostaglandin E2 and enprostil. We conclude that at least a component of the secretory inhibition by enprostil reflects direct interference with histamine stimulation of parietal cell adenylate cyclase.

1-Methyl-3-isobutylxanthine↗
PubMed1993

Stimulatory (EP1 and EP3) and inhibitory (EP2) prostaglandin E2 receptors in isolated ileal smooth muscle cells.

Isolated smooth muscle cells from the circular layer of pig and guinea-pig ileum were used to study the effect of prostaglandin E2 (PGE2) and three PGE2 receptor (EP) agonists; iloprost (EP1), butaprost (EP2) and enprostil (EP3). In pig cells, PGE2 and enprostil induced cell contraction (22.1 and 21.5% shortening of cell length, obtained at 10 nM for PGE2 and 1 nM for enprostil, respectively). Iloprost and butaprost had no contractile effect. However, the cholecystokinin octapeptide (CCK-8; 10 nM)-induced contraction was inhibited when cells were preincubated with iloprost or butaprost. In guinea-pig cells, PGE2, butaprost and iloprost induced cell contraction, whereas enprostil had no effect (23.1% for 10 nM PGE2, 22.8% for 1 nM butaprost and 22.6% for 10 nM iloprost). Preincubation with SC19220 (EP1 antagonist) inhibited the PGE2-, butaprost- and iloprost-induced contractions. When the contractile effect of PGE2, butaprost and iloprost was inhibited by addition of SC19220, these agents inhibited the cell contraction induced by CCK-8 (1 nM). Smooth muscle cells from guinea-pig and pig ileum express two PGE2 receptor subtypes that induce opposite effect. EP1 and EP3 receptors mediate cell contraction in guinea-pig and pig, respectively, whereas EP2 receptors mediate cell relaxation in both species.

Alprostadil↗
PubMed1988

Prostanoid inhibition of canine parietal cells: mediation by the inhibitory guanosine triphosphate-binding protein of adenylate cyclase.

We have investigated the mechanisms underlying prostaglandin inhibition of histamine-stimulated parietal cell function. Enzyme-dispersed canine parietal cells were enriched by elutriation. The accumulation of the weak base [14C]aminopyrine was used as an index of parietal cell function and cyclic adenosine monophosphate content was measured by radioimmunoassay. Step density gradients of the elutriator-enriched parietal cell fractions indicated that parietal cells accounted for the histamine stimulation of cyclic adenosine monophosphate production and inhibition by the prostaglandin E analogue Enprostil. Pertussis toxin adenosine diphosphate-ribosylates a subunit with a molecular weight of 41,000, thereby inactivating the inhibitory guanine nucleotide-binding protein of adenylate cyclase. Pertussis toxin treatment of parietal cells in overnight suspension culture was used to determine if inhibitory guanosine triphosphate-binding protein mediated prostanoid inhibition. In control cultured cells, prostaglandin E2 and Enprostil markedly inhibited forskolin- and histamine-stimulated aminopyrine accumulation. In parietal cells treated with pertussis toxin (300 ng/ml) for 18 h, stimulation of parietal cell function by histamine, isobutylmethylxanthine, and forskolin was unaltered compared with control cells, whereas prostaglandin E2 and Enprostil inhibition was markedly reduced. In pertussis toxin-treated cells, histamine-stimulated cyclic adenosine monophosphate generation was unaltered, whereas Enprostil inhibition of histamine-stimulated cyclic adenosine monophosphate production was markedly reduced. Pertussis toxin treatment of membranes from control, but not from pertussis toxin-treated, cells induced the [32P]adenosine diphosphate-ribosylation of a membrane protein with a molecular weight of 41,000, presumably the alpha-subunit of inhibitory guanosine triphosphate-binding protein. We conclude that prostanoids inhibit parietal cell function by receptor-mediated interaction with the inhibitory guanine nucleotide-binding protein of adenylate cyclase.

Adenosine Diphosphate Ribose↗
PubMed1995

Copresence of prostaglandin EP2 and EP3 receptors on gastric enterochromaffin-like cell carcinoid in African rodents.

BACKGROUND & AIMS: Prostaglandins (PGs) have important roles in the regulation of gastric acid secretion. The aim of this study was to examine the possible presence of PG receptors on the gastric enterochromaffin-like (ECL) carcinoid of Mastomys natalensis, which might be a useful model of normal ECL cells. METHODS: A [3H]PGE2 binding experiment was performed by using the ECL tumor membrane, and intracellular signal transduction was studied in the cells. In addition, Northern blot analysis using EP2 and EP3 receptor complementary DNAs was conducted. RESULTS: [3H]PGE2 specifically bound to the tumor cell membrane, and the binding was displaced by various PGs with a potency order of PGE1 = PGE2 > enprostil > PGF2 alpha. Although PGE1 and PGE2 stimulated 5'-cyclic adenosine monophosphate (cAMP) production, neither PGF2 alpha nor enprostil had any effect. On the other hand, all of PGE1, PGE2, PGF2 alpha, and enprostil attenuated the forskolin-induced cAMP production. Moreover, enprostil inhibited histamine release induced by forskolin. However, on pertussis toxin treatment, PGE2 paradoxically enhanced the forskolin-induced increase of cAMP production. Finally, the presence of EP2 and EP3 receptor messenger RNAs was confirmed by RNA blot analysis. CONCLUSIONS: The ECL carcinoid tumor cells of Mastomys seem to possess two subtypes of PGE receptor: EP2 linked to cAMP production and EP3 coupled with inhibitory guanosine 5'-triphosphate-binding proteins mediating the inhibition of cAMP production.

Animals↗
PubMed1995

Cholinergic stimulatory effect of intragastric administration of a prostaglandin E2 analogue on pancreatic exocrine secretion in conscious rats.

The effect of a long-acting, potent synthetic analogue of prostaglandin E2, enprostil, on pancreatic exocrine secretion was examined in conscious rats. Rats were prepared with cannulae draining bile and pancreatic juice separately. Pancreatic exocrine secretion was increased by intragastric administration of enprostil but inhibited by its intravenous administration. The pancreatic response to intragastric administration of enprostil was not inhibited by the administration of cholecystokinin antagonist or secretin antibody, or by bilateral vagotomy, but was completely abolished by atropine. Therefore, intragastric administration of enprostil seemed to stimulate pancreatic exocrine secretion via a peripheral gastro-(entero)-pancreatic reflex.

Amylases↗