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)

We have devised an improved high pressure liquid chromatographic technique whereby serotonin, nucleosides, cyclic nucleotides, namely cAMP and cGMP, and 5'mono-, 5'di-, and 5'tri-nucleotides can be analyzed. The cyclic nucleotides have been measured in picomolar quantities. All nucleotides can be quantitated in a single step separation in 75 min using a 0.0015 M phosphoric acids vs. 1M pH 4.8 ammonium phosphate gradient. 5/10 ml of platelet-rich plasma furnishes an adequate sample for complete analysis. Nucleotide levels in platelets from 16 normal donors expressed in 10(11) platelets are as follows: cAMP, 6.32 (4.15) nanomoles and AMP, 0.32 (0.14); ADP, 2.48 (0.67); ATP 3.78 (0.68); GDP 0.38 (0.07) and GTP, 0.45 (0.07) micromoles. ADP and ATP values are lower than those previously published. However, the total nucleotide level approaches published values. Upon aggregation with thrombin, approximately 50% of ADP and 40% ATP is releaseed. Release is complete by 2 min. Thrombin is the most potent releasing agent with collagen and ADP occupying an intermediate role and epinephrine being the least effective. Upon aggregation cyclic AMP levels diminish along the other nucleotides. Patients with asthma showed depression of ADP, ATP, GDP and GTP levels.
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PMID:Measurement of nucleotide pools in platelets using high pressure liquid chromatography. 57

During pentobarbital (25 mg/kg i.v. in 2 min), pentothal (15 mg/kg i.v. in 2 min) and ketamine (10 mg/kg i.v. in 2 min) narcosis, rabbits showed reduced platelet reactivity ot the direct aggregating effect of ADP (2 X 10(-5) M) and the indirect effect of thrombin (0.1 U/ml). Certain arousal drugs, specifically those of metabolic type such as SAMe (20 mg/kg i.v. in 2 min) and Thiola (166 mg/kg i.v. in 2 min) and of haemodynamic type such as nicergoline (6.66 mg/kg i.v. in 2 min) and hexobendine (5 mg/kg i.v. in 2 min) administered 31 min after narcosis induction, impede the depression brought on by narcosis on on platelet reactivity.
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PMID:[Narcosis, platelet aggregation and arousing drugs]. 68 73

Treatment of 24 male patients with 3 g/day of xanthinol nicotinate did not change the in vitro measurements of ADP-induced platelet aggregation but produced a marked inhibition of collagen-induced platelet aggregation. This effect may be connected with the drug-induced depression of the ATP level in platelet-rich plasma. Changes in the platelets in the patients' blood or in the lipid composition and the concentration of uric acid in their serum were ruled out as reasons for the decrease of the collagen-induced aggregation. The activity of the three serum enzymes y-GT, GOT, and GPT and the concentration of the blood sugar did not change.
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PMID:Effect of xanthinol nicotinate treatment on platelet aggregation. 84 33

At time of admission 50 hospitalized male patients assigned to one of two groups judged as depressed and nondepressed completed one form of the Depression Adjective Check List (DACL). Depressed patients were placed in a highly specific treatment regime: Antidepressive program (adp), which required display of assertive behavior for termination of treatment. After removal from the program ADP patients received an alternate form of the DACL, and 2 weeks postadmission all patients completed a third form of testing. Significant decrease in number of dysphoric mood items selected posttreatment was found for the ADP group as compared with nondepressed patients. Lower depression scores were obtained after ADP across the period studied. Length of time in ADP was related negatively to initial depression scores. Results are interpreted in terms of reinforcement contingencies that sustain depressive verbal behavior.
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PMID:Effects of antidepressive program on verbal behavior. 85 98

The effects on myocardial function, metabolism and ultrastructure of 60 minutes of reperfusion, instituted after 30, 60 and 90 minutes of occlusion of the left anterior descending coronary artery, were studied in 48 dogs. Twelve sham-operated dogs served as controls. Coronary occlusion for 60 or 90 minutes caused significant depression in the first derivative of left ventricular pressure (dP/dt) (P less than 0.05) that could not be reversed by reperfusion. Upon reperfusion, creatine phosphate stores in myocardium made ischemic for 30 and 60 minutes, but not for 90 minutes, returned toward control levels, but stores of adenosine triphosphate (ATP) and total nucleotides and the ATP/adenosine diphosphate ratio of myocardium subjected to 60 and 90 minutes of ischemia were further decreased. After 60 and 90 minutes of ischemia, swelling of the sarcoplasmic reticulum and mitochondrial damage (swelling, decreased matrix density and partial loss of cristae) were seen. Myofibrils were relaxed in all these groups. Reperfusion produced gross contraction of myofibrils and aggravated these changes in mitochondria and sarcoplasmic reticulum. In the hearts subjected to 90 minutes of ischemia these changes were gross. The levels of creatine phosphokinase, glutamic oxaloacetic transaminase and lactic dehydrogenase in the coronary sinus blood increased dramatically (P less than 0.05) upon reperfusion after 60 or 90 minutes of occlusion, indicating severe impairment of cell membranes. This secondary rise in serum enzyme activity during reperfusion should be taken into consideration when estimating the size of a myocardial infarct from enzyme changes alone. It appears that 60 and 90 minutes of ischemia cause severe myocardial damage that is not reversed by reperfusion maintained for 1 hour although longer periods of reperfusion may be beneficial.
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PMID:Alterations in energy metabolism and ultrastructure upon reperfusion of the ischemic myocardium after coronary occlusion. 108 Mar 52

Oxidative phosphorylation was measured polarographically in mitochondria isolated from rat heart. With regard to ADP/O ratio and respiratory control index, no differences were found among mitochondria isolated from normal, acutely (increased pneumatic resistance of the heart-lung preparation) and chronicly (renal hypertension) stressed heart. However, the acute stressed heart induced by strangulating the outflow tract of the heart-lung preparation showed clear depression and tendency to depression, respectively, in the level of ADP/O ratio and respiratory control index in mitochondria. The results indicate that there is no change in the oxidative phosphorylating mechanism of the myocardial mitochondria of nonfailed heart despite acute or chronic pressure loadings; however, there is an uncoupling of oxidative phosphorylation in mitochondria of the failed heart after acute strangulation of the outflow tract.
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PMID:Oxidative phosphorylation in mitochondria isolated from stressed rat heart. 121 39

Rats aged 7, 30 days and 3-5 months were given intraperitoneally single doses (2.5 mg/kg) of reserpine. The content of the adenyl system compounds (ATP, ADP, AMP and inorganic phosphorus) was determined. It was shown that as regards the extent of ATP and ADP depression the 7-day old animals proved more sensitive to reserpine than were adult animals.
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PMID:[Age-related characteristics of the reaction of the myocardial adenyl system to pharmacological sympatholysis]. 122 80

1 The interaction of effects between 5-hydroxytryptamine (5-HT) and adenosine diphosphate (ADP) on human or rabbit platelets was investigated in vitro. The initial platelet shape change and their aggregation were measured in stirred, citrated platelet-rich plasma (PRP) at 37 degrees C by recording the rate and extent of changes in light scattering and light transmission. 2 Both the velocity and extent of aggregation and the velocity and extent of the rapid morphological change caused by ADP were enhanced by simultaneous addition of 5-HT. Methysergide but not imipramine inhibited the 5-HT effects. 3 Platelets were made refractory to the aggregating and shape changing effect of either ADP or 5-HT by repeated aggregation with the particular agent; platelets made refractory to ADP retained their responsiveness to 5-HT and platelets made refractory to 5-HT responded to ADP. Platelets pre-incubated for 3-10 min with 5-HT without aggregation showed greatly reduced aggregation on subsequent addition of ADP. Methysergide inhibited all the effects of 5-HT whilst imipramine was inactive. 4 When the shape change or aggregation of platelets induced by ADP was submaximal, addition of 5-HT increased it further. Pre-incubation of PRP with 5-HT before the addition of ADP resulted in failure of the secondary induction of aggregation or shape change by 5-HT. The secondary induction by 5-HT also did not occur in the presence of methysergide; imipramine had no inhibitory effect. Similar secondary induction of aggregation was shown by adrenaline injected during aggregation by ADP; the adrenaline effect was removed by phentolamine but not by propranolol. 5 Our results show that the initial change in shape of platelets and their aggregation can be induced by ADP or 5-HT in specific manner. The interaction of the effect of these substances on platelets can result in either increase in platelet sensitivity or, under certain conditions, decrease in platelet responsiveness. The increase or depression of platelet reactivity appears to be a highly specific effect and is probably mediated at specific receptors involved with platelet activation.
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PMID:Shape change and aggregation of blood platelets: interaction between the effects of adenosine and diphosphate, 5-hydroxytryptamine and adrenaline. 125 69

Adenosine and adenine nucleotides [adenosine-5'-monophosphate, adenosine-5'-diphosphate, adenosine triphosphate (ATP), cyclic adenosine 3',5'-monophosphate (dbcAMP)], but not (cAMP) and dibutyryl cyclic adenosine 3',5'-monosphosphate (dbcAMP)], but not adenine or inosine, inhibited the twitch response of the electrically stimulated guinea-pig myenteric plexus-longitudinal muscle preparation. With each agent except dbcAMP, inhibition was manifest muscle preparation. With each agent except dbcAMP, inhibition was manifest from 1 to 500 muM was maximal within 1 minute. For dbcAMP, higher concentrations were required (10-fold increase) and inhibition was maximal after 20 to 30 minutes. Theophylline (0.05-0.5 mM) both reversed and prevented the inhibition produced by each of these agents. In higher concentrations (greater than 1 mM), theophylline itself depressed the twitch response. Neither propranolol nor phenoxybenzamine altered theophylline-induced depression, whereas phenoxybenzamine did not alter adenosine-induced inhibition. Adenosine, ATP, cAMP and theophylline (0.25 mM) did not alter acetylcholine-induced contractions, whereas a higher concentration of theophylline (2.5 mM) inhibited contractions. Theophylline (up to 0.5 mM) did not antagonize epinephrine- or dopamine-induced inhibition of the twitch response, but did antagonize morphine-induced inhibition. These findings suggest that adenosine and related nucleotides act at a common receptor site at which theophylline acts as a competitive antagonist and that there is a link between morphine and adenine nucleotide action in this preparation.
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PMID:Inhibition of acetylcholine release from cholinergic nerves by adenosine, adenine nucleotides and morphine: antagonism by theophylline. 127 Dec 86

The present study investigated whether reduced adenylate cyclase activity and an increase in inhibitory guanine nucleotide binding proteins (Gi alpha), which have been observed in the failing human heart, already occur in myocardial hypertrophy before the stage of heart failure. In membranes of hypertrophic hearts from rats with different forms of experimentally induced hypertension without heart failure (one-kidney, one clip rats, deoxycorticosterone-treated rats, and rats with reduced renal mass), basal as well as isoprenaline-, 5'-guanylylimidodiphosphate-, and forskolin-stimulated adenylate cyclase activity was reduced. The activity of the catalyst was depressed in deoxycorticosterone but unchanged in one-kidney, one clip and reduced renal mass compared with controls. The number of beta-adrenergic receptors was similar in all groups. Radioimmunological quantification of Gi alpha proteins revealed an increase by 73% in one-kidney, one clip, 67% in reduced renal mass, but only 20% in deoxycorticosterone compared with sham-operated, age-matched control rats. The increase of Gi alpha was accompanied by smaller changes of pertussis toxin-induced [32P]ADP-ribosylation of a 40-kd membrane protein. It is concluded that Gi alpha contributes to the reduced adenylate cyclase activity in cardiac hypertrophy in one-kidney, one clip and reduced renal mass and to a smaller extent in deoxycorticosterone. It is suggested that an enhanced expression of Gi alpha could occur not only in severe heart failure but also in cardiac hypertrophy and could, therefore, contribute to myocardial depression and progression of disease in heart failure. In addition, Gi alpha might represent an important regulatory mechanism for cardiac adenylate cyclase activity and thus, might play an important role in various cardiac diseases.
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PMID:Desensitization of adenylate cyclase and increase of Gi alpha in cardiac hypertrophy due to acquired hypertension. 131 58


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