Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The dose-related antianesthetic and antidotal property of dibutyryl cyclic AMP, devoid of toxic effects, imparts uniqueness to the nucleotide as an arousal agent. Of the analeptic drugs studied (d-amphetamine, picrotoxin, pentylenetetrazol, caffeine, theophylline, strychnine, ethamivan and doxapram), only picrotoxin demonstrated antianesthetic properties. However, picrotoxin was associated with severe toxicity at all dose levels tested. No analeptic drug is effective in reversing the central nervous system depression produced by sedative, hypnotic or tranquilizer drug overdosage.
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PMID:Comparisons between the antianesthetic action of dibutyryl cyclic AMP and analeptic drugs on amobarbital-induced narcosis in the rat. 0 96

The influence of an anaesthetic dose of chlormethiazole (Hemineurin) on blood flow (CBF) and oxygen consumption (CMRO2) in the rat brain was investigated. In spontaneously breathing animals a dose of 160 mg . kg-1 of chlormethiazole, infused i.v., induced a state close to surgical anaesthesia. In paralyzed animals, the same dose decreased CBF and CMRO2 to about 60% of control, an effect similar to that observed after an anaesthetic dose of phenobarbitone. Neither a protective nor a detrimental effect of chlormethiazole could be demonstrated when the drug was given during reversible and pronounced, incomplete ischaemia, as evaluated from the postischaemic tissue concentrations of labile phosphates (PCr, ATP, ADP, AMP) and of lactate and pyruvate. It is concluded that protection in this situation (as earlier shown with phenobarbitone) must, at least partly, be related to other mechanisms than a depression of metabolism.
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PMID:Influence of chlormethiazole on cerebral blood flow and oxygen consumption in the rat, and its effect on the recovery of cortical energy metabolism after pronounced, incomplete ischaemia. 3 16

Previous studies had suggested that the epileptic bursts of feline generalized penicillin epilepsy represent the response of hyperexcitable cortex to thalamocortical volleys normally evoking spindles. If this were the case, it should be possible to convert the epileptic bursts of generalized penicillin epilepsy into spindles by decreasing the excitability of cortical neurons. In cats exhibiting the EEG signs of feline generalized penicillin epilepsy cortical excitability was decreased by hypoxia, by the topical application to the cortex of KCl (inducing spreading depression), barbiturates, GABA, AMP or noradrenaline. During generalized penicillin epilepsy, hypoxia and KCl-induced spreading depression abolished epileptic bursts which were replaced by spindles. When spindles and epileptic complexes occurring in the same animal were compared, a direct correlation between the frequencies of these two rhythms could be demonstrated, that of the epileptic complexes being about half that of the spindle waves. These observations support the hypothesis that the epileptic bursts of feline generalized penicillin epilepsy are induced by thalamocortical volleys normally involved in spindle genesis. Topical cortical applications of barbiturates, GABA, AMP and noradrenaline reduced or inverted the negative spikes of the spike and wave complexes, while augmenting the negative slow waves, or revealing them clearly in instances in which they had been poorly developed. This effect is interpreted as being due to a selective inactivation of the superficial cortical layers. That topical cortical application of barbiturates, GABA, AMP and noradrenaline was capable of transforming into typical spike and wave complex epileptic bursts, which had not previously conformed to this pattern, indicates that the intracortical electrophysiological events of typical and atypical epileptic bursts in feline generalized penicillin epilepsy are fundamentally the same and reflect an alternation between excitatory and inhibitory sequences.
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PMID:Effects of changes in cortical excitability upon the epileptic bursts in generalized penicillin epilepsy of the cat. 8 21

High doses of propranolol give rise to a liver disenzymic injury by depression of its clearance and colloidopexic functions, but without any histological change. The molecular target responsible for this disturbance seems to lie at the level of ATP-ase, because propranolol stimulates the membrane activity and supresses the citochondrial one. There are described some effects of this drug and its pharmocological opposite, isopropylenorepinephrine, on the liver cell enzymes, which may serve as a morphological proof of the antagonism between the mitochondrial and plasmalemal ATP-ase activity, on the one hand, and of the membrane ATP-ase and AMP-cyclase, on the other hand.
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PMID:Dynamic aspects of the liver ATP-ase and its functional involvement in propranolol treated rat. 12 89

The present study was carried out to examine the possible intervention of some hormones in the "protein-sparing/actions of dietary carbohydrate and fat. Administration of either a carbohydrate meal or a fat meal to fasted rats caused a reduction in the urinary output of urea and total nitrogen with a concomitant decrease in rate of urogenesis in liver. as well as the activities of some amino acid-catabolizing enzymes in liver. The sparing action of carbohydrate but not that of fat was abolished in alloxan-diabetic rats. Feeding rats a carbohydrate meal caused a marked reduction in the amount of cyclic AMP in liver. The change was coincident with a reduction in the level of plasma urea and the urinary output of urea and total nitorgen. Administration of dibutyryl cyclic AMP abolished the carbohydrate-induced depression of urinary output of urea and total nitrogen as well as partially the activity of serine dehydratase in liver. Feeding a carbohydrate meal resulted in a significant reduction in the level of corticosterone in plasma. However, the possible intervention of glucocorticoids in the protein-sparing action of carbohydrate was ruled out inasmuch as the action of carbohydrate was also observed in the adrenalectomized rats. The overall results suggest that the protein-sparing action of dietary carbohydrate may be exerted in a different fashion from that of fat, that is, through depression of cyclic AMP in liver and thus the reduction of the degradation of amino acids in liver
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PMID:Possible intervention of insulin, cyclic AMP, and glucocorticoids in protein-sparing action of dietary carbohydrate in rats. 16 49

The effects of verapamil on myocardial isometric force on contraction, cardiac adenosine 3,'5'-monophosphate (cyclic AMP) and heart phosphorylase alpha activity were studied in the isolated perfused rat heart. When hearts were perfused with verapamil (5.98 times 10- minus 8 M), force of contraction was reduced approximately 50% within 4 to 5 minutes; at this point, the concentration of cyclic AMP was significantly lower than control but phosphorylase alpha activity was unchanged. In hearts perfused continuously for 60 minutes with verapamil, force of contraction and cyclic AMP levels returned to normal within 20 minutes after administration of verapamil was begun. Isoproterenol (0.355 nmol/min) reversed the depressant effect of verapamil on cardiac contractility and restored heart cyclic AMP levels to normal. Methoxamine (35.5 nmol/min) given to verapamil-depressed hearts, caused contractile force to return to normal, but cardiac cyclic AMP levels remained low. Mephentermine (23.0 nmol/min) had no effect on cardiac contraction, cyclic AMP or phosphorylase alpha activity in hearts depressed by verapamil. It was concluded that with the concentration of verapamil used in these experiments, the drug caused a transient decrease in force of contraction and myocardial cyclic AMP. Both the depression in myocardial contractility and in cardiac cyclic AMP caused by verapamil were reversed promptly by isoproterenol, whereas methoxamine overcame acutely only the negative inotropic effect of verapamil. Mephentermine had no effect on hearts depressed by verapamil.
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PMID:Effects of verapamil on myocardial contractility, cardiac adenosine 3,'5'-monophosphate and heart phosphorylase. 16 48

Lithium (Li+) chloride, 2 to 3 mEq. per kilogram of body weight, was administered intraperitoneally to normal Wistar rats daily for 4 to 66 days. This resulted in a marked reduction in urine osmolality (Uosm.) and increase in the excretion of water, Na+, K+, uric acid, and phosphate. The excretion of uric acid and potassium was a direct function of UNaV. The magnitude of depression in urine osmolality was significantly related to the rate of excretion of lithium in the urine, suggesting that the change in water reabsorption is dependent on the presence of the ion in the luminal side of the tubule. During 2 per cent saline diuresis, Li+-treated rats achieved less fractional free water reabsorption (TcH2O/GFR times 100) at any level of fractional osmolar clearance (Cosm./GFR times 100) than normal rats. On the other hand, during 0.225 per cent saline diuresis, fractional free water clearance (CH2O/GFR times 100) was normal over a wide range of fractional urine flow (V/GFR times 100), indicating intact function of the ascending limb of the loop of Henle. The intravenous infusion of vasopressin (VP) or dibutyryl cyclic-adenosine monophosphate (dcAMP) to Li+-treated rats resulted in a modest rise in Uosm. and a reduction in V/GFR times 100 and CH2O/GFR times 100. Although the response to VP appeared earlier than that to dibutyryl cyclic-AMP, the magnitude of the changes in Uosm., V/GFR times 100, and CH2O/GFR times 100 was eventually the same with both substances. Comparison between normal and Li+-treated rats revealed that the response to both VP and dibutyryl cyclic-AMP was blunted, albeit to a greater extent in the former. Inhibition by Li+ of adenylate cyclase will only partially explain the present data. Impairment in the release of endogenous VP or a block distal to the formation of cyclic-AMP must have played a role. In view of a normal diluting capacity and the increase in the excretion of phosphate and uric acid, it is suggested that Li+, when administered chronically in the present doses, inhibits proximal tubular reabsorption.
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PMID:Renal effects of lithium administration in rats: alterations in water and electrolyte metabolism and the response to vasopressin and cyclic-adenosine monophosphate during prolonged administration. 16 79

1 N-2-O-dibutyryl adenosine 3',5'-monophosphate (db cyclic AMP), adrenaline and aminophylline produce a potentiation of the tension developed (Td) and the maximum rate of rise of tension (dT/dt max) in the rat isolated diaphragm during indirect electrical stimulation. Aminophylline and db cyclic AMP also produce the same effect during direct stimulation. 2 Propranolol produced a depression of the action of adrenaline on Td and dT/dt max during indirect stimulation of the diaphragm. On the other hand, the potentiating actions of db cyclic AMP and of aminophylline on Td and dT/dt max during indirect stimulation were unaffected by propranolol. 3 The results support the idea that cyclic AMP may be involved not only in regulating the processes associated with synthesis, mobilization and storage of transmitter in the motor nerve terminal, but also in modifying some metabolic processes which regulate the function of the contractile elements.
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PMID:The effects of cyclic N-2-O-dibutyryl- adenosine 3',5'-monophosphate, adrenaline and aminophylline on the isometric contractility of the isolated hemidiaphragm of the rat. 16 33

The effect of verapamil on myocardial contractility, heart adenosine 3', 5'-monophosphate (cyclic AMP) and cardiac phosphorylase a activity was studied in isolated perfused rat hearts. In a concentration of 0.025 mug/ml, verapamil decreased force of contraction 50% and caused a significant fall in heart cyclic AMP within 4 to 5 min after perfusion with the drug was begun. When perfusion of the heart with medium containing verapamil was continued for 60 min, contractile force gradually returned to control. at the end of 60 min of perfusion with verapamil, the myocardial concentration of cyclic AMP was not different from that measured in hearts perfused with contro medium for a similar time period. Isoproterenol, given at the point of maximal contractile depression induced by verapamil, restored normal force of contraction and raised cardiac cyclic AMP to the same level as that observed when the catecholamine was given to untreated hearts; When methoxamine was administered to hearts depressed by verapamil, contractility returned to normal, but cyclic AMP content remained below control values.
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PMID:Metabolic and inotropic effects of verapamil in perfused rat heart. 17 69

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


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