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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

By determining glycogen synthetase activity, rate of 14C-glucose incorporation and glycogen levels, using pharmacologic agents which act on the alpha, beta M and N receptors, the influence of the autonomic system on synthesis of this polysaccharide in heart and skeletal muscle was analysed. The results indicate that the autonomic system is involved in intracellular autoregulation of glycogen synthetase activity through tissue receptors. Drugs which stimulate the cholinergic system depress this enzyme activity in the heart and skeletal muscle indirectly by releasing endogeneous catecholamines (nicotine-gangliconic effect) and also inhibit utilization of energetic ATP and phosphocreatinine reserves in the heart (muscarinic effect). Stimulation of the alpha-adrenergic receptor enhances glycogen anabolism in both types of muscles depending on the stimulatory influence of nonsterified sugers released in the process of glycogen hydrolysis and depression of cAMP level and presence of glucosteroids. Stimulation of beta-adrenergic receptors induces opposite changes. Analysis of the influence of pharmacologic agents that stimulate and inhibit decomposition and synthesis of glycogen showed that hydrolytic decomposition is probably one of the main processes of intracellular autoregulation of glycogen synthetase activity.
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PMID:The role of receptors of the autonomic system in regulation of glycogen synthetase activity in the heart and skeletal muscle in rats. 11 45

The effect of hypoxia on glycogen content, adenyl cyclase activity, cyclic 3',5'-AMP concentration, lactate: pyruvate ratio and the energy charge potential connected with the pool of adenylates was evaluated in the motor area of the cortex of beagle dogs. At first, controlled hypoxia induces activation of the adenyl cyclase system while subsequently, with PaO2 values lower than 20 mm Hg, a depression of the system is observed simultaneously with a drop of the energy charge potential. When normal oxygenation is resumed, the biochemical parameters examined tend to go back to normal even though it is still necessary to resort to anaerobic mechanisms. The intracarotid perfusion with nicergoline enhances the post-hypoxic recovery of adenyl cyclase activity, even though the ergoline derivative is inactive during the stages of hypoxic suffering of the brain studied in the present work.
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PMID:Effect of hypoxia on the cerebral energy state. 16 98

The significance of Ca++ for glucose stimulation of insulin release was studied in an in vitro system with beta-cell-rich pancreatic islets microdissected from oh/ob-mice. There was only a slight depression of cAMP in islets exposed to the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine after withdrawal of Ca++ from the incubation medium. The lack of a stimulatory effect of glucose noted in the absence of extracellular Ca++ is therefore probably accounted for by factors other than impaired adenylate cyclase activity. A rise of extracellular Ca++ above the concentration necessary for obtaining the optimal secretagogic effect of glucose resulted in inhibition of the glucose-stimulated insulin release, leaving basal secretions and islet contents of cAMP unaffected. Evidence was provided in support of the idea that H+ completes for Ca++ in glucose stimulation of insulin release. Both the rate of basal insulin release and that seen after stimulation with glucose were diminished by about 50% after introducing 0.2 mM La+++ in the incubation medium. These observations emphasize the significant role of Ca++ in the regulation of insulin secretion, suggesting that not only a decrease but also an increase of the functionally important intracellular pool(s) of Ca++ can result in a diminished response to glucose.
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PMID:The significance of calcium for glucose stimulation of insulin release. 16 23

Cyclic AMP and its dibutyryl derivative inhibit neuronal firing of the labellar sugar sensitive receptor of the blowfly when applied in conjunction with the stimulant sucrose. Furthermore, simultaneous application of aminophylline (phosphodieterase inhibitor) and sucrose or in combination with cyclic AMP caused a similar depression of the sugar receptors response. In contrast, dibutyryl cyclic GMP elicited an increase in sugar receptor firing when applied with sucrose to sugar receptor. Either 5'-AMP or 5'-GMP in combination with sucrose had no discernable effect on the sugar receptors response. Different ratio combinations of cyclic AMP and dibutyryl cyyclic GMP showed the striking inhibitory effect of cyclic AMP upon the dibutyryl cyclic GMP elicited increases in receptor firing frequency. Therefore, it is suggested that these two nucleotides may be mediating different but complimentary aspects of sugar receptor function in a push-pull manner.
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PMID:Apparent opposing effects of cyclic AMP and dibutyryl cyclic GMP on the neuronal firing of the blowfly chemo-receptors. 18 Oct 76

This research examined the effects of several cyclic nucleotides on in vivo cat soleus nerves and muscles. The reagents were administered by rapid close intra-arterial injection while electrical activity in single motor axons and contractile activity in the whole muscle were monitored. Cyclic N6-2'-O-dibutyryl adenosine 3',5'-monophosphate (dibutyryl cAMP) initiated bursts of action potentials in unstimulated axons. It also caused the occurrence of stimulus bound repetitive potentials in stimulated axons. It caused the muscle to undergo a series of rapid asynchronous contractions and potentiated the strength of stimulus-evoked contractions. Monobutyryl cAMP produced similar responses, but was less potent than dibutyryl cAMP. cAMP produced only a small, transient depression of neuromuscular transmission. There was no response to dibutyryl cyclic 3',5' guanosine monophosphate or sodium butyrate. None of these reagents affected denervated muscle. The results suggest that cAMP-like materials that can penetrate nerve membranes cause depolarization of motor nerve terminals, prolongation of the depolarization of the terminal initiated by an action potential and release of transmitter.
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PMID:Effects of cyclic nucleotides on mammalian motor nerve terminals. 18 84

Cyclic AMP (cAMP) was determined in that part of the rat cerebral cortex which was invaded by slow potential change (SPC) accompanying cortical spreading depression (CSD). cAMP was determined at various phases of SPC development and at several time intervals after SPC recovery. At maximum SPC, cAMP was increased by 100% above control and by 116% at the time of SPC recovery. Five, 10 and 15 min after SPC recovery, +54%, +34% and 0% increase in cAMP was found, respectively. The activity of phosphorylase a increased by 112% at SPC recovery (maximal cAMP increase), and by 13% 15 min later (complete cAMP recovery). Some depolarizing agents which differ in their ability to stimulate cAMP formation in vitro (veratridine, cyanide and glutamate) when applied topically onto the cerebral cortex in concentrations evoking CSD (2 mM veratridine, 10 mM cyanide and 100 mM glutamate), induced uniform increase of cAMP by about 100%. The same cAMP augmentation was found in the cortical region under maximum SPC induced by these agents.
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PMID:Brain cyclic adenosine 3',5'-monophosphate during depolarization of the cerebral cortical cells in vivo. 18 23

The effects of mannoheptulose and DL-glyceraldehyde on glucose-induced insulin release and cycli AMP levels in islets isolated from rat pancreas were investigated. Mannoheptulose inhibition on glucose-induced insulin release was observed after only 5-min incubation period, indicating an inhibitory effect on the early phase of insulin release. This inhibition on insulin release was accompanied with the simultaneous depression of cyclic AMP levels in islets. By the addition of DL-glyceraldehyde to the medium in which glucose and mannoheptulose were present, the depressed cyclic AMP levels in islets were recovered to the control level completely but the restoration of insulin release in the early phase was not complete. In the absence of glucose, DL-glyceraldehyde did not demonstrate a significant increase of insulin release during 5 min incubation, though a marked stimulation was observed after 30-min incubation. Cyclic AMP levels in islets were not affected by DL-glyceraldehyde. When DL-glyceraldehyde was added to the medium with glucose, significant inhibition of glucos-induced insulin release in its early phase was observed without the reduction of cyclic AMP levels in islets. From these findings, the following possibilities are suggested and discussed. 1. Maintenance of the cyclic AMP levels in islets is a necessary but insufficient condition for glucose-induced insulin release particularly for its early phase. 2. Glucose-induced insulin release seems to depend on both the binding of glucose with glucoreceptor and the supply of some metabolites. Mannoheptulose inhibits both mechanisms. DL-glyceraldehyde may supply metabolites but competitively inhibit the binding of glucose to the glucoreceptor.
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PMID:Effects of mannoheptulose and DL-glyceraldehyde on glucose induced insulin release and adenosine 3',5'-monophosphate levels in isoalted islets of rat pancreas. 18 34

Adenosine depressed norepinephrine contractions of dogs' saphenous vein strips in both the presence and the absence of Ca2+ and after inhibition of calcium influx by verapamil. It antagonized noncompetitively contractions induced by Ca2+ in depolarized strips after alpha-adrenergic blockade. Contractions obtained with acetylcholine were also depressed by adenosine. This depression was not accompanied by an increase in cAMP or a decrease in the elevated cGMP level. Thus the depression of the smooth muscle cell reactivity still occurs in the absence of calcium influx and is not mediated by the cyclic 3',5'-nucleotide system. Adenosine diphosphate and triphosphate, but not adenosine (10(-6) to 10(-4) M), increased the basal tension of resting saphenous strips. This was prevented by removal of calcium from the bath. In contracted strips, lower concentrations of both nucleotides (10(-6) to 10(-5) M) caused relaxation whereas with high concentrations (10(-4) to 10(-3) M) further contraction occurred. Thus, unlike adenosine, the adenine nucleotides facilitate calcium influx.
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PMID:Action of adenosine and adenine nucleotides on dogs' isolated veins. 19 78

Short term in vitro experiments showed that, added alone, verapamil inhibited both glycolysis and Ca uptake in embryonic chicken and rat bone cells. Added together with PTH, verapamil (0.02 MM) enhanced cAMP production, had no effect on lactate production, but significantly inhibited citrate, calcium and phosphate release from embryonic rat and mouse calvaria incubated under hypocalcemic conditions. The depression by verapamil of PTH-stimulated demineralization was confirmed histologically. It is concluded that in addition to cAMP, Ca plays a key role in the action of PTH on bone.
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PMID:The effect of verapamil on the action of parathyroid hormone on embryonic bone in vitro. 20 Apr 41

ACTH, cholera toxin, cyclic AMP but not pregnenolone-induced steroidogenesis in Y-1 functional mouse adrenal tumor cells was significantly inhibited by delta-9-tetrahydrocannabinol, cannabidiol, and cannabinol. The inhibition of steroidogenesis could not be correlated with a general depression in cell function or viability. The data suggest that cannabinoids inhibit corticosteroidogenesis at a site between the synthesis of cAMP and of pregnenolone.
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PMID:Inhibition of cortiocosteroidogenesis by delta-9-tetrahydrocannabinol. 20 49


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