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At least 19 recordsLinked to original sources
PubMed1978

The role of various prostaglandins on the correlation between permeability to albumin and cAMP levels in the isolated mesentery.

Prostaglandins (PG) have been shown to raise the level of cyclic AMP (cAMP) in various tissues, and to increase permeability. Whether both events are linked, is at present a matter of speculation. We have investigated the effects of PGE1, E2, A1, A2, F1alpha and F2alpha on an isolated rat mesentery placed in a diffusion cell (surface area : 2 sq.cm). The PGs (5 microgram/ml) increased the passage of (I 125) - Albumin across the mesentery. In other experiments, diks of rat mesentery (surface area : 2 sq.cm) have been incubated in assay tubes, and cAMP levels measured by a binding protein assay. We have observed an excellent correlation between increases in permeability and cAMP levels (r=0.961). In order of increasing potency on both parameters, the PGs may be classified as follows : PGF, PGA and PGE. In the rat mesentery, under the influence of prostaglandins, increases in permeability and in cAMP levels are apparently connected.

Albumins↗
PubMedDate not supplied

Effects of some prostaglandins on the main phosphorylating, electron transporting and peroxidative systems of the erythrocyte membrane.

Investigations regarding the main biochemical systems of the erythrocyte membrane were performed on rat erythrocyte ghosts after treating the animals with PGA1, PGE1 and PGF2alpha. These investigations have shown that the prostaglandins which were found to induce changes in the erythrocyte flexibility (PGE1 and PGF2ALPHA) also induce significant changes in the concentrations of lipid peroxides, SH groups, proteins and nicotinamide adenine nucleotides, as well as in the activity of some electron transportors belonging to the nicotinamide proteins, in the erythrocyte membrane.

Adenine Nucleotides↗
PubMed1978

Actions of prostaglandins on isolated perfused cat coronary arteries.

Effects of prostaglandins on coronary arterial smooth muscle were studied in isolated perfused cat coronary arteries. This preparation was shown to be responsive to known vasoactive agents, including angiotensin II, adenosine, and norepinephrine. Prostaglandins E2 and F2 alpha (PGE2 and PGF2 alpha) produced dose-dependent coronary arterial constriction at concentrations of 3 times 10(-9) M or greater. PGE1 produced a biphasic dose-response curve with constriction at low concentrations greater than 10(-7) M.PGI2 dilated coronary arteries at concentrations greater than 10(-8) M. Inhibition of endogenous prostaglandin synthesis with meclofenamate potentiated responses to prostaglandins. The endoperoxide, PGH2, slightly constricted cat coronary arteries. However, in the presence of human platelet microsomes, PGH2 was converted to thromboxane A2(TxA2), which was the most potent coronary artery constrictor among the naturally occurring compounds studied. Analysis of coronary artery perfusate for TxB2 confirmed the thromboxane generation, which was markedly lower in the presence of imidazole. Two synthetic endoperoxide analogs produced potent coronary arterial constriction. Induction of hypoxia to a PO2 of 50 mmHg or increasing basal tome with 30 mM KCl did not diminish coronary artery response to prostaglandins, suggesting that prostaglandins released from ischemic myocardial tissue may influence coronary arterial tone.

Animals↗
PubMed1978

Antidipsogenic role of the E-prostaglandins.

Prostaglandin E1 (PGE1) is antidipsogenic when administered into the lateral cerebral ventricle of the rat. In these experiments PGE1, at a dose of 1 microgram, suppressed water intake induced by centrally administered angiotensin II (AII) or carbachol, subcutaneously administered polyethylene glycol, and water deprivation. Even at this high dose, PGE1 did not reduce water intake due to cellular dehydration. As the dose of PGE1 was reduced, its suppressant effects became more specific to AII-induced drinking, with a dose of 10 ng yielding a significant suppression only in the case of AII-induced drinking. Even at a high dose (1 microgram), the PGE1 suppression of ingestion was specific to water intake. Although PGE1-treated rats reduced food intake if they were not hydrated prior to access to food, no reduction in food intake was seen when they received water by gavage before food presentation. Since PGE-like substances are synthesized in the brain, these data suggest the possibility that the prostaglandin may be involved in the regulation of water balance as a component of a reciprocal system in which water intake initiated by the activation of the renin-angiotensin system is halted by the synthesis and release of PGE.

Angiotensin II↗
PubMed1979

The use of immobilized ligands and [125I]protein a for immunoassays of thromboxane B2, prostaglandin D2, 13,14-dihydro-prostaglandin E2, 5,6-dihydro-prostaglandin I2, 6-keto-prostaglandin F1 alpha, 15-hydroxy-9 alpha, 11 alpha(epoxymethano)prosta-5,13-dienoic acid and 15-hydroxy-11 alpha,9 alpha(epoxymethano)prosta-5,13-dienoic acid.

Immunoassays were developed for quantitative determination of thromboxane B2, prostaglandin D2, 13,14-dihydro-prostaglandin E2, 5,6-dihydro-prostaglandin I2, 6-keto-prostaglandin F1 alpha, 15-hydroxy-9 alpha, 11 alpha (epoxymethano) prosta-5, 13-dienoic acid and 15-hydroxy-11 alpha, 9 alpha (epoxymethano) prosta-5,13-dienoic acid. Ligands immobilized by covalent linkage to a solid support, bound homologous rabbit antibodies. [125I] Protein A was used to measure the bound IgG antibody. Increments of homologous and heterologous fluid-phase ligand completed with solid-phase ligand for antibody and resulted in decreasing amounts of bound [125I]-Protein A. The serologic specificity for each immune system was determined. Immunoassays for thromboxane B2, 6-keto-prostaglandin F1 alpha, and 5,6-dihydro-prostaglandin I2 were used to identify their respective homologous ligands that were separated by normal phase and reversed phase high pressure liquid chromatography.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1979

The effects of synthetic prostaglandin analogs on canine hepatic bile flow.

The synthetic prostaglandin analogs 16, 16-dimethyl PGF2 alpha and 16, 16-dimethyl PGE2 were administered to dogs with chronic biliary and gastric fistulas. The effects of 16, 16 diMePGF2 alpha and 16, 16 diMePGE2 were evaluated on bile flow and composition and bile adenosine 3', 5' monophosphate (cyclic AMP) secretion. 16, 16 diMePGF2 alpha in doses of 0.125 and 0.25 microgram-kg-min significantly increased hepatic bile flow. The choleresis was characterized by increased chloride and bicarbonate secretion. Measurement by radioimmunoassay of bile cyclic AMP concentration demonstrated no evident increase in bile cyclic AMP secretion associated with the choleresis produced by 16, 16 diMePGF2 alpha. The administration of 16, 16 diMePGE2 in a dose range 0.01 to 1.0 microgram-kg-min did not significantly alter bile flow rates or composition. Bile erythritol-14C clearance, a measure of canalicular bile flow, was significantly increased by PGF2 alpha but not by 16, 16-dimethyl PGF2 alpha, suggesting that the mechanism of action of PGF2 alpha in stimulating hepatic bile flow may be different from that involved in 16, 16-dimethyl PGF2 alpha choleresis. The results of this study indicate that the synthetic PGF2 alpha analog produces a choleretic response not mediated by adenylate cyclase and associated with increased chloride and bicarbonate secretion.

16,16-Dimethylprostaglandin E2↗
PubMed1979

Ovarian activity, and total gonadotrophin and gonadotrophin releasing hormone levels in response to some synthetic non-steroidal ovulating agents in the catfish, Heteropneustes fossilis (Bloch).

Effects of clomiphene citrate, cyclofenil and prostaglandins (PGE1 and PGF2 alpha) on ovarian 32P uptake, on gonadotrophin levels in the pituitary gland and blood serum and on a gonadotrophin releasing hormone-like (GnRH-like) substance in the hypothalamus were investigated in Heteropneustes fossilis. These drugs were very effective in increasing the serum level of gonadotrophin with a subsequent increase in ovarian 32P uptake in sham-hypophysectomized recipients. All the drugs except cyclofenil failed to stimulate 32P incorporation by the ovary in hypophysectomized fish. Clomiphene citrate and cyclofenil also induced a significant increase in the GnRH-like factor in the hypothalamus of H. fossilis. Such a response was not obtained in fish treated with PGE1 and PGF2 alpha. It seems likely that the action of clomiphene is routed through the hypothalamo-pituitary-ovarian axis and that of prostaglandins directly through the pituitary-ovarian axis. The action of cyclofenil is bimodal; one effect like that of clomiphene and the other direct upon the ovary probably by increasing its sensitivity to the available gonadotrophin.

Animals↗
PubMed1978

Kinetics of aggregation of human platelets.

A study of the aggregation kinetics of human platelets using an electronic counting device is reported. The experimental data were analyzed quantitatively by a physical model, which assumed that the initial disappearance rate of single platelets versus time fitted a second-order type of aggregation with respect to platelet number. The mechanism of aggregation was surface barrier controlled. Thus, the aggregation rate constants in different adenosine diphosphate concentrations (1.5-9.0 microgram) were 10-100 times greater than the rate constant (6.6325 x 10(-12) cm3/sec) for a diffusion-controlled mechanism, were smaller in the surface-barrier-controlled process and ranged from 0.00741 to 0.0467. The extent of aggregation was indicated by the calculation of a sticking probability constant as determined by the barrier. Adenosine diphosphate induced a rapid aggregating effect. Prostaglandin E1 produced the most drastic deaggregating effect as compared to dinoprostone (prostaglandin E2) and dinoprost (prostaglandin F2alpha). Aspirin completely blocked the aggregating effect of arachidonic acid.

Adenosine Diphosphate↗
PubMed1978

The localization of a histamine H2-receptor adenylate cyclase system in canine parietal cells and its inhibition by prostaglandins.

A method is described for the preparation of parietal cell-enriched suspensions from dog gastric mucosa. Histamine and E type prostaglandins produce an elevation of cyclic AMP concentration in mixed cell preparations. Parietal cell-rich fractions respond to histamine but only weakly to prostaglandins whilst in fractions virtually free from parietal cells the converse is observed. Prostaglandins which are good antisecretory agents, PGE1, PGE2 and 16,16 dimethyl PGE2 are potent inhibitors of the histamine elevations of cyclic AMP in parietal cell-rich fractions, whilst PFG2alpha shows 1% of their potency. The experiments described support the view that histamine stimulates gastric acid secretion by excitation of an H2-receptor adenylate cyclase system in the plasma membrane of the parietal cell and that acid secretory inhibition by prostaglandins is a result of inhibition of that system.

Adenylyl Cyclase Inhibitors↗
PubMed1978

Prostaglandin I2 is less relaxant than prostaglandin E2 on the lamb ductus arteriosus.

Prostaglandin (PG) I2 and its stable metabolite, 6-keto-PGF1alpha, were tested on the isolated ductus arteriosus from mature fetal lambs. PGI2 relaxed the ductus in high doses (threshold 10(-6)M) and its activity disappeared on standing at room temperature for 30 minutes. 6-keto-PGF1alpha was inactive at all doses. By contrast, PGE2 produced a dose-dependent relaxation over a range between 10(-10) and 10(-6)M. These findings confirm that PGE2 is the most potent ductal relaxant among the known derivatives of arachidonic acid. PGE2 probably maintains ductus patency in the fetus and, together with PGE1, remains the compound of choice in the management of newborns requiring a viable ductus for survival.

Animals↗
PubMed1978

Low prostaglandin concentrations cause cardiac rhythm disturbances. Effect reversed by low levels of copper or chloroquine.

In perfused male rat hearts concentrations of prostaglandins (PGs) E2 and F2alpha in the range 1 pg/ml to 10 ng/ml (2.8 X 10(-12) to 2.8 X 10(-8)M) consistently caused rhythm irregularities. Higher concentrations had no effect themselves and stabilized rhythm in hearts made unstable by lower concentrations. Copper ions (as the sulphate) at 2 X 10(-6)M stabilized hearts made unstable by PGs and when present prior to the PGs prevented PG induced disturbances. Chloroquine also reversed PG-induced rhythm changes.

Animals↗