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At least 1,531 records · Page 85Linked to original sources
PubMed1975

Inhibition of lipolysis and cyclic AMP accumulation in white fat cells by tetracycline.

The effects of tetracycline on the metabolism of isolated rat white fat cells were examined. Tetracycline at a concentration of 0.05 mg/ml inhibited lipolysis due to 0.075 or 0.15 muM norepinephrine, but not that due to adenosine deaminase, theophylline, dibutyryl cyclic AMP or 1.5 muM norepinephrine. Higher concentrations of tetracycline (1 mg/ml) inhibited lipolysis due to all added agents except dibutyryl cyclic AMP. The accumulation of cyclic AMP after 5 minutes incubation with 0.15 muM norepinephrine plus adenosine deaminase was inhibited by 0.05 mg/ml of tetracycline. The large rise in cyclic AMP accumulation at 5 minutes due to 1.5 muM norepinephrine in the presence of 100 muM theophylline was only slightly inhibited by 0.05 or 0.1 mg/ml of tetracycline. Tetracycline at 1 mg/ml did markedly inhibit cyclic AMP accumulation due to all added agents. The stimulation of adenylate cyclase activity of fat cell ghosts by norepinephrine or fluoride was inhibited by 0.05 mg/ml or greater concentration of tetracycline. Insulin-stimulated glucose oxidation by fat cells was inhibited by 1 mg/ml of tetracycline. These results suggest that the anti-lipolytic action of tetracycline on rat fat cells is secondary to inhibition of cyclic AMP accumulation.

Adenylyl Cyclase Inhibitors↗
PubMed1991

Modulation of nicotinic acetylcholine receptors by intracellular calcium and cyclic AMP in Lymnaea stagnalis neurones.

Acetylcholine (ACh)-receptor ion channels were investigated under the modulatory action of calcium and cyclic AMP in completely isolated Lymnaea stagnalis neurones using the noise analysis technique. Elevation of the intracellular Ca2+ concentration in dialyzed neurones produced a reduction in the amplitude of ACh induced current accompanied by slight decrease in the mean channel open time and a simultaneous 1.5-fold increase in mean channel conductance. Direct introduction of cyclic AMP into neurones or elevation of intracellular cyclic AMP level by application of serotonin or forskolin produced 20-40% reduction in ACh-induced conductance without significant effect on the measured parameters of the ion channels. The inhibitory effects of calcium and cyclic AMP appear to be independent. Our findings indicate that reduction in ACh induced conductance under calcium and cyclic AMP modulation results from an alteration in the channel gating mechanism. Since the efficiency of ion transfer is independent of cyclic AMP, and it even rises with the elevation of calcium concentration, the inhibition of ACh responses may be accounted for by a decrease in the rate constant for channel opening, so that channels activated by acetylcholine remain in a closed state over longer intervals.

Animals↗
PubMedDate not supplied

[Fluorimetric ultramicrodetermination of the dansyl derivatives of cyclic 3'5-AMP by thin-layer chromatography].

A new fluoriemtric ultramicromethod was developed for quantiative determination of cyclic 3',5'-AMP as derivative of dansyl chloride using silica gel thin-layer chromatography. In presence of dansyl chloride cyclic 3',5'-AMP formed a fluorescent complex. A spot of dansyl derivative of cyclic 3',5'-AMP was photographed on a reversible colour film, after which the colour intensity of the spot on the film was determined directly by a special densitometer. Content of cyclic 3',5'-AMP was studied in different regions of rat brain. The in fluence of some psychotropic drugs on the level of cyclic 3',5'-AMP was studied using this method. The method was highly sensitive and reproducible and enabled to determine 10(-10) -- 10(-11) M cyclic 3',5'-AMP.

Chromatography, Thin Layer↗
PubMed1976

The effect of histamine, isoproterenol and tyramine on rat uterine cyclic AMP.

Isoproterenol (10(-4) M), histamine (10(-3) M) and tyramine (10(-3) M) elevated cyclic AMP levels in incubated rat urerine segments. Promethazine (10(-6) M) an H1-receptor antagonist was ineffective in blocking the increase in cyclic AMP due to isoproterenol, histamine and tyramine. Buriamide (10(-6) M), an H2 receptor antagonist, was effective in almost abolishing the cyclic AMP elevation due to histamine, whereas burimamide did not affect the cyclic AMP levels elevated by tyramine and only slightly reduced the isoproterenol response. Propranolol was effective in reducing or abolishing the cyclic AMP accumulation by all three agonists. The respective blockade by burimamide or propranolol was overcome by increasing the concentration of the agonists. Histamine (10(-3) M) and tyramine (10(-3) M) failed to elevate cyclic AMP in uterine segments obtained from reserpine treated rats. The data supports the hypothesis that histamine, like tyramine, has an indirect effect on the rat uterus mediated through the release of endogenous norepinephrine.

Animals↗
PubMed1975

LH and FSH stimulation of cyclic AMP in specific cell types isolated from the testes.

The direct effect of LH and FSH on cyclic AMP levels in specific cell types, isolated from the rat testes, was investigated in vitro. LH significantly stimulated cyclic AMP production in isolated interstitial cells and had only a slight effect on the isolated germ cells. FSH significantly stimulated cyclic AMP production in isolated seminiferous tubules, organ cultures of testes explants, and isolated Sertoli cells, with only a small response elicited in the germ cells. FSH had no effect on the cyclic AMP levels in interstitial cells and either freshly isolated or cultured peritubular cells. These data indicate that the Sertoli cells and interstitial cells are the main cell types in the testes which respond to FSH and LH respectively with increased cyclic AMP production. A possible slight effect of either hormone on the cyclic AMP level in the germ cells has not be ruled out.

Animals↗
PubMed1976

Effect of narcotic dependence and withdrawal on striatal dopamine-sensitive adenylate cyclase and synaptosomal cyclic AMP metabolism.

In rats rendered tolerant to the dependent on morphine, striatal cyclic AMP metabolism was significantly enhanced as reflected by elevated cyclic AMP levels and adenylate cyclase activity. Following withdrawal from morphine treatment, whereas the activity of straital adenylate cyclase was significantly reduced when compared to morphine-dependent rats, the drop in cyclic AMP was not significant. Although addition of dopamine (40 muM) stimulated equally well the striatal adenylate cyclase from control or morphine-dependent animals, the activity of dopamine-stimulated enzyme was blocked in animals undergoing withdrawal. The crude synaptosomal fraction of the whole brain obtained from morphine-dependent rats exhibited an even more pronounced increase in cyclic AMP which was accompanied by elevated adenylate cyclase and protein kinase activity. Naloxone administration suppressed this rise in cyclic AMP and reversed the morphine-stimulated increases in adenylate cyclase and protein kinase. Following the withdrawal of morphine treatment, alterations in cyclic AMP metabolism were similar to those noted for the morphine-naloxone group.

Adenylyl Cyclases↗
PubMed1976

Cyclic AMP and bicarbonate responses of the dog pancreas to vasoactive intestinal peptide (VIP) and secretion.

The effects of secretin (3 CU per kilogram) and vasoactive intestinal peptide (VIP; 8 mug per kilogram) on bicarbonate and cyclic AMP secretions in pancreatic juice (with pancreatic duct perfusion) and on pancreatic tissue cyclic AMP were investigated as a function of time in 13 anesthetized dogs. The peptides were given by rapid intravenous injection. Even 30 sec. after peptide administration, tissue cyclic AMP levels were elevated, reaching peak values within the first minute and a second peak at about 3 min. Bicarbonate and cyclic AMP secretions in pancreatic juice started with a lag of 1 min. after peptide injection. Following the injection of VIP, peak pancreatic response developed within the first 5 min. and the pancreatic response actually disappeared after 15 min., whereas secretion evoked by secretin was sustained for at least 30 min. The mean +/- S.D. observed maximal bicarbonate response to VIP (100 +/- 49 muEq./5 min.) was about one sixth of the maximum output following secretin (592 +/- 181 muEq./5 min.). Increases in pancreatic tissue and juice cyclic AMP caused by VIP were significant (p less than 0.05) at 1 and 4 min.; however, they were but moderate if compared with the rise achieved by secretin. The results presented confirm previous reports that VIP is a secretin-like partial agonist of pancreatic bicarbonate secretion and are compatible with the hypothesis that both secretin and VIP elicit canine pancreatic bicarbonate secretion via the second messenger system of cyclic AMP.

Animals↗
PubMed1976

Stimulation of Ca2+ uptake by cyclic AMP and protein kinase in sarcoplasmic reticulum-rich and sarcolemma-rich microsomal fractions from rabbit heart.

The effect of cyclic AMP on Ca2+ uptake by rabbit heart microsomal vesicular fractions representing mainly fragments of either sarcoplasmic reticulum or sarcolemma was investigated in the presence and absence of soluble cardiac protein kinase and with microsomes prephosphorylated by cyclic AMP-dependent protein kinase. The acceleration of oxalate-promoted Ca2+ uptake by fragmented sarcoplasmic reticulum following cyclic AMP-dependent membrane protein phosphorylation, observed by other authors, was confirmed. In addition it was found that the acceleration was greatest at pH 7.2 and almost negligible at pH 6.0 and pH 7.8. A very marked increase in Ca2+ uptake by cyclic AMP-dependent membrane protein phosphorylation was observed in the presence of boric acid, a reversible inhibitor of Ca2+ uptake. In addition to the microsomal fraction thought to represent mainly fragments of the sarcoplasmic reticulum, the effect of protein kinase and cyclic AMP on Ca2+ uptake was investigated in a cardiac sarcolemma-enriched membrane fraction. Ca2+ uptake by sarcolemmal vesicles, unlike Ca2+ uptake by sarcoplasmic reticulum vesicles, was inhibited by low doses of digitoxin. The acceleration of oxalate-promoted Ca2+ uptake by cyclic AMP and soluble cardiac protein kinase, however, was quite similar to what was seen in preparations of fragmented sarcoplasmic reticulum, which suggests that it may reflect an acceleration of active Ca2+ transport across the myocardial cell surface membrane.

Animals↗
PubMed1977

Studies on the mechanisms of somatostatin action on insulin release. IV. effect of somatostatin on cyclic AMP levels and phosphodiesterase activity in isolated rat pancreatic islets.

The effects of somatostatin on insulin release and cyclic AMP metabolism were studied in collagenase-isolated islets of Langerhans from the rat. Ceoncentrations from 500 to 2000 ng/ml significantly inhibited glucose stimulated insulin release, while 100 and 200 ng/ml were ineffective. Somatostatin (2000 ng/ml) inhibited insulin release and [3H]-cyclic AMP accumulation induced by 16.7 mM glucose after 10 and 30 min of incubation. In dose-response studies, the inhibition by somatostatin of the effect of glucose on [3H]cyclic AMP and insulin release could be overcome by a high concentration of the hexose (44.9 mM), suggesting competitive inhibition. In the absence of glucose, somatostatin inhibited [3H]cyclic AMP accumulation induced by the phosphodiesterase inhibitor, IBMX, while no inhibition was seen, again in the absence of hexose, when the [3H]cyclic AMP levels had been raised by the adenyl cyclase stimulator, cholera toxin. Somatostatin did not affect phosphodiesterase activity when added to islet homogenates, but preincubation of the islets with the peptide before homogenization decreased the activity by about 30%. It is suggested that somatostatin-induced inhibition of insulin release is, at least partially, mediated by cyclic AMP, probably through an action on islet adenyl cyclase.

Adenylyl Cyclases↗
PubMed1977

Effects of cobalt-60 gamma-irradiation in association with prostaglandin E1 treatment on the cyclic AMP levels of some radiosensitive tissues.

The amounts of cyclic AMP in brain, liver and intestinal mucosa have been measured in rats, at constant intervals, up to 18 days after whole-body exposure to either a unique moderate dose (500 rd) or a unique lethal dose (750 rd) of cobalt-60 gamma-radiation in association with a preliminary intraperitoneally treatment with prostaglandin E1 (5 microgram/100 g body weight/day) during five days. The amounts of tissular cyclic AMP in these two experimental groups were compared with those obtained from control groups identically irradiated or treated with prostaglandin E1. The effects of gamma-irradiation and prostaglandin E1 treatment on the cyclic AMP levels were found to be quite specific in these organs, suggesting that they contain different adenyl cyclase-cyclic AMP-phosphodiesterase systems: a cerebral system which is influenced by both gamma-radiation and prostaglandin E1, a hepatic system which is "radioresistant" and an intestinal system which is not influenced by prostaglandin E1. When associated with gamma-radiation, this prostaglandin is capable, on the one hand, to annul the "radioresistance" of the hepatic cyclic AMP system and, on the other hand, to annul the "radiosensitivity" of the intestinal cyclic AMP system.

Animals↗
PubMed1978

Effect of thyroid hormone, actinomycin D, cycloheximide and puromycin on TRH-induced secretion of TSH, as studied by pituitary concentration of cyclic AMP and intrathyroidal colloid droplet formation.

In an attempt to study the functional relation between pituitary cyclic AMP and TSH secretion in response to thyrotropin releasing hormone (TRH) or thyroid hormone administration, pituitary concentration of cyclic AMP was measured by protein binding assay after in vivo and in vitro administration of test materials (TRH, thyroxine, triiodothyronine, actinomycin D, puromycin and cycloheximide singly or in combination). Small dose of TRH apparently augmented TSH secretion as evidenced by a marked increase of intrathyroidal colloid droplet, but failed to elevate the pituitary concentration of cyclic AMP. Triiodothyronine (T3) and thyroxine (T4) blocked an increase of TSH secretion produced by TRH, but they elevated pituitary concentration of cyclic AMP in vivo and in vitro. Actinomycin D (Act D), puromycin and cycloheximide elevated pituitary cyclic AMP concentration without stimulating TSH secretion. From the data accumulated, it appears that the measurement of total anterior pituitary concentration of cyclic AMP is not useful to evaluate the activity of TSH cells in response to thyroid hormone, TRH and TRH plus thyroid hormone.

Animals↗
PubMed1978

Inhibition of plasminogen activator secretion by cyclic AMP in a macrophage-like cell line.

The continuous cell line, J774.2, exhibits many macrophage-like functions such as latex and Fc-mediated phagocytosis, antibody mediated phagocytosis, antibody mediated cytotoxicity, chemotaxis, and lysozyme secretion. Cyclic AMP stimulates Fc-mediated phagocytosis and inhibits the growth of J774.2. To further evaluate the relationship between cyclic AMP and the specialized functions exhibited by these cells. Variants deficient in phagocytosis, adenylate cyclase and cyclic AMP-dependent protein kinase were derived. We have now shown that J774.2 also secretes plasminogen activator and that this secretion is rapidly and specifically inhibited by 8-bromoadenosine 3':5'-cyclic monophosphoric acid (8 Br--cAMP) or cholera toxin under conditions where lysozyme secretion is unaltered. Utilizing protein kinase-deficient variants, the ability of cyclic AMP to inhibit plasminogen activator secretion was shown to be mediated by a cyclic AMP-dependent protein kinase. We conclude that cyclic AMP has diametrically opposing effects on two macrophage-like functions: Fc-mediated phagocytosis and plasminogen activator secretion.

Animals↗
PubMed1979

Polyoma virus and cyclic AMP-mediated control of dihydrofolate reductase mRNA abundance in methotrexate-resistant mouse fibroblasts.

As a model cell culture system for studying polyoma-mediated control of host gene expression, we isolated methotrexate-resistant 3T6 cells in which one of the virus-induced enzymes, dihydrofolate reductase, is a major cellular protein. In highly methotrexate-resistant cell lines dihydrofolate reductase synthesis accounts for over 10% that of soluble portein, corresponding to an increase of approximately 100-fold over the level in parental cells. This increase in dihydrofolate reductase synthesis is due to a corresponding increase in the abundance of dihydrofolate reductase mRNA and gene sequences. We have used these cells to show that infection with polyoma virus results in a 4- to 5-fold increase in the relative rate of dihydrofolate reductase synthesis and a corresponding increase in dihydrofolate reductase mRNA abundance. The increase in dihydrofolate reductase synthesis begins 15 to 20 h after infection and continues to increase until cell lysis. These observations represent the first direct evidence that viral infection of eukaryotic cells results in the increased synthesis of a specific cellular enzyme and an increase in the abundance of a specific cellular mRNA. In order to gain additional insight into the control of dihydrofolate reductase synthesis we examined other parameters affecting dihydrofolate reductase synthesis. We found that the addition of fresh serum to stationary phase cells results in a 2-fold stimulation of dihydrofolate reductase synthesis, beginning 10 to 12 h after serum addition. Serum stimulation of dihydrofolate reductase synthesis is completely inhibited by the presence of dibutyryl cyclic AMP as well as by theophylline or prostaglandin E1, compounds which cause an increase in intracellular cyclic AMP levels. In fact, the presence of dibutyryl cyclic AMP and theophylline results in a 2- to 3-fold decrease in the rate of dihydrofolate reductase synthesis and the abundance of dihydrofolate reductase mRNA. However, in contrast to the effect on serum stimulation, dibutyryl cyclic AMP and theophylline do not inhibit polyoma virus induction of dihydrofolate reductase synthesis or dihydrofolate reductase mRNA levels. These observations suggest that dihydrofolate reductase gene expression is controlled by at least two regulatory pathways: one involving serum that is blocked by high levels of cyclic AMP and another involving polyoma induction that is not inhibited by cyclic AMP.

Bucladesine↗
PubMed1978

Effect of cyclic AMP on transformation and proliferation of leishmania cells.

A correlation between cyclic AMP (adenosine 3' : 5'-monophosphate) concentration within Leishmania cells and proliferation and transformation is demonstrated. By addition of dibutyryl cyclic AMP and cyclic AMP-phosphodiesterase inhibitors to the culture medium the intracellular level of cyclic AMP was increased. In the presence of 1mM caffeine the level of cyclic AMP accumulated in L. tropica promastigotes from 90 pmoles up to 380 pmoles per 10(9) cells, whereas the proliferation rate decreased to 50%. In the case of L. donovani the transformation of amastigotes to promastigotes was inhibited by addition of dibutyryl cyclic AMP as well as caffeine and papaverine. Especially caffeine (2mM) and papaverine (0.1mM) reduced the transformation rate to less than 5% after 48 h, compared to 35% of the control.

Bucladesine↗
PubMed1979

Regulation of phosphatidylcholine metabolism by cyclic AMP in a model alveolar type 2 cell line.

The influence of cyclic AMP on the metabolism of phosphatidylcholine, the major component of pulmonary surfactant was examined in a cell line (A549) with type 2 pneumonocyte characteristics. It was found that cyclic AMP increased both the total amount of phosphatidylcholine and disaturated phosphatidylcholine as well as the incorporation of [3H]choline into these fractions. The effect was specific for cyclic AMP since 5'-AMP, adenosine, and cyclic GMP did not alter phosphatidylcholine or disaturated phosphatidylcholine levels. Cyclic AMP had no effect on phosphatidylcholine and disaturated phosphatidylcholine metabolism in another non-type 2 human epithelial cell line (MA-160). Since the ability of various cyclic AMP analogs to increase phosphatidylcholine and disaturated phosphatidylcholine levels was correlated with their ability to activate protein kinase, it seems likely that a protein phosphorylation mechanism is involved in controlling phosphatidylcholine metabolism.

Animals↗
PubMed1979

Urinary cyclic AMP and cyclic GMP in normal and asthmatic subjects during exercise.

The purpose of this study was to compare exercise-induced changes in urinary cyclic AMP and cyclic GMP of normal and asthmatic subjects. All subjects were exercised to 80% of predicted maximum heart rate for 15 minutes on a bicycle ergometer. FEV1 was measured before and after exercise to determine the degree of bronchoconstriction due to exercise. Five urine specimens were collected by voluntary voiding at 20 minute intervals (one specimen before exercise and four after exercise). Before exercise, the asthmatic subjects excreted less cyclic GMP (p less than 0.05) but the same cyclic AMP as the normal subjects. Creatinine excretion in nine asthmatic subjects decreased by 24% (p less than 0.01) during exercise. In sixteen normal subjects (post-exercise bronchoconstriction less than 10%) cyclic AMP excretion increased by 19% (p less than 0.05) within 20 minutes after exercise, while cyclic GMP excretion did not change significantly. In thirteen asthmatic subjects (post-exercise bronchoconstriction greater than 20%) cyclic AMP excretion did not change significantly, while cyclic GMP excretion increased by 23% (p less than 0.05) within 20 minutes after exercise. This study has shown that exercise affects the excretion of cyclic AMP, cyclic GMP, and creatinine in normal and asthmatic subjects. The response of normal and asthmatic groups to exercise was the same for creatinine but different for cyclic AMP and cyclic GMP.

Adolescent↗
PubMed1985

Short term and long term effects of beta-adrenergic effectors and cyclic AMP on nitrendipine-sensitive voltage-dependent Ca2+ channels of skeletal muscle.

The effects of short term stimulation of beta-adrenergic receptors and elevations in intracellular cyclic AMP on nitrendipine-sensitive voltage-dependent Ca2+ channels of skeletal muscle cells in vitro has been studied using both the 45Ca2+ flux technique and [3H] nitrendipine-binding experiments. Isoproterenol increased the nitrendipine-sensitive 45Ca2+ influx under depolarizing conditions. The effects of isoproterenol were additive to those of depolarization and were antagonized by alprenolol. Half-maximal inhibition of 45Ca2+ influx induced both by depolarization and by isoproterenol occurred at a nitrendipine concentration of 1 nM. Treatments that resulted in an increased level of intracellular cyclic AMP, such as treatment with 1-methyl-3-isobutylxanthine, theophylline, dibutyryl cyclic AMP, or 8-bromocyclic AMP also resulted in an increased rate of 45Ca2+ entry via nitrendipine-sensitive Ca2+ channel. In contrast, long term treatment of myotubes in culture with isoproterenol and other compounds that increased intracellular cyclic AMP led to a large increase in the number of nitrendipine receptors. This increase was accompanied by a 4-10-fold decrease in the affinity of the receptors for nitrendipine. Alprenolol inhibited the long term effects of isoproterenol. In vivo treatment of 7-day-old chicks with reserpine and alprenolol produced a decrease in the number of skeletal muscle nitrendipine receptors. This decrease in receptor number was accompanied by an increase in the affinity of nitrendipine for its receptor by a factor of 4 to 5. These effects on the nitrendipine receptor were prevented by simultaneous injection of isoproterenol. The results are discussed in relation to the role of beta-adrenergic receptors and intracellular cyclic AMP in the regulation of skeletal muscle Ca2+ channels.

1-Methyl-3-isobutylxanthine↗
PubMed1975

Modulators of cyclic AMP systems.

On the basis of the data reported here, one may conclude that although many agents that act in the central nervous system are modulators of the action of cyclic AMP, it is difficult to establish a direct connection between the pharmacologic activity and the levels of cyclic AMP in the brain. This lack of interrelation applies to the benzodiazepines as well as to the pyrazolopyridines. The data for members of the latter group are somewhat frustrating in this regard, since an excellent correlation has been shown to exist between the potency of inhibition of PDE and activity in the antianxiety test. In measurements of steroidogenesis in the isolated adrenal cell, the correlation between activity in vito and the conflict assay is even better. The data presented here and reported elsewhere (Shimizu et al., 1974; Kelly et al., 1974; Mayer and King, 1974; King and Mayer, 1974) provide evidence that agents that act as inhibitors of PDE in cell-free systems exert their influence on cyclic AMP in tissue slices of the brain of guinea pigs by mechanisms that seem not to be related to an effect on PDE. Papaverine, and possibly chlordiazepoxide, may act by releasing agonists that, in turn, stimulate the accumulation of cyclic AMP. This activity is blocked bo other inhibitors of PDE, such as theophyline. Results obtained by the use of platelets are refreshingly clear. Inhibition of aggregation has been shown to occur when the level of cyclic AMP is raised, and a suggestive exists that the most potent inhibitors of platelet PDE are the best potentiators of the action of PGE1 in blocking aggregation. The study utilizing drugs collected from a large number of therapeutic classes makes clear that it is difficult to attribute the mechanism of action for any of the classes studied to modulation of cyclic AMP. An unexpected finding of this study, however, was the fact that pharmacologic agents include an unusually large number of inhibitors of PDE as compared with agents chosen at random. This finding provides a powerful tool for the biochemical pharmacologist who is examining large numbers of compounds in the search for potential drugs.

Adenylyl Cyclase Inhibitors↗