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 effects of four progestational agents pregnenolone sulphate, cyproterone acetate, norethindrone acetate and progesterone, on adenosine-evoked depression of the firing of rat cerebral cortical neurones have been studied. When applied iontophoretically, pregnenolone sulphate, cyproterone, and norethindrone enhanced the actions of iontophoretically applied adenosine and failed to potentiate the depressant effects of adenosine 5'-N-ethylcarboxamide and gamma-aminobutyric acid. Cyproterone acetate (50 micrograms kg-1) and progesterone (200 micrograms kg-1) administered intravenously enhanced the depressant actions of iontophoretically applied adenosine. When applied by large currents, cyproterone, and less frequently norethindrone, depressed the firing of cerebral cortical neurones. The depressant effects of cyproterone were antagonized by caffeine. Pregnenolone sulphate tended to excite cortical neurones but neither this action, nor its potentiation of adenosine were reproduced by application of sulphate ions. It is hypothesized that some of the psychotropic actions of progestational agents may involve an enhancement of 'purinergic' tone in the central nervous system.
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PMID:Potentiation of the depression by adenosine of rat cerebral cortical neurones by progestational agents. 381 5

The effects of the novel thromboxane A2 (TXA2) antagonists, ONO-1270 and ONO-3708, on the electrical and mechanical responses evoked by various agents, and in particular 9,11-epithio-11,12-methano-thromboxane A2 (STA2), were investigated in the guinea-pig artery. STA2 (up to 0.3 microM), and ONO-1270 and ONO-3708 (up to 1.0 microM) did not modify the membrane potential in smooth muscle cells. Perivascular nerve stimulation induced an excitatory junction potential (e.j.p.), and with frequencies over 0.25 Hz, depression of e.j.ps occurred. STA2 (0.1 microM) and both ONO-1270 and ONO-3708 had no effect on these electrical events. STA2 (over 0.1 microM) produced phasic and tonic contractile responses, in a concentration dependent manner. Both ONO-1270 and ONO-3708 competitively inhibited the phasic contraction induced by STA2 as estimated from parallel shifts in the dose-response curve, and from the Lineweaver-Burk and Schild plots (the PA2 values were 8.22 for ONO-1270 and 8.70 for ONO-3708), but both agents inhibited non-competitively the PGF2 alpha-induced contraction. ONO-1270 and ONO-3708 (up to 0.1 microM) had no effect on contractions induced by K+ and caffeine, but did slightly inhibited contractions induced by 5-hydroxytryptamine (5-HT). Following application of indomethacin, neither agent modified the 5-HT-induced contraction. In Ca2+-free solution, 10 nM STA2 produced a phasic but not a tonic contractile response. ONO-1270 and ONO-3708 (over 1 nM) inhibited this phasic contractile response.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Actions of the novel thromboxane A2 antagonists, ONO-1270 and ONO-3708, on smooth muscle cells of the guinea-pig basilar artery. 382 37

The acute effects of coffee on exercise-induced angina were studied in 17 men with coronary artery disease using a double-blind treadmill protocol. Ingestion of either 1 or 2 cups of caffeinated coffee increased the exercise duration until onset of angina (8 and 12%, respectively, p less than 0.05), whereas decaffeinated coffee had no effect. The extent of ST-segment depression and the heart rate-blood pressure product at angina were similar after drinking caffeinated and decaffeinated coffee. Exercise duration until 0.1 mV of ST-segment depression, as well as the heart rate, blood pressure and double product at angina and at 0.1 mV of ST-segment depression were similar after drinking caffeinated or decaffeinated coffee. The mean serum caffeine levels (+/- standard deviation) after ingestion of 1 and 2 cups of caffeinated coffee were 1.97 +/- 1.0 and 3.89 +/- 1.6 micrograms/ml, respectively. The acute ingestion of 1 to 2 cups of caffeinated coffee had no deleterious effect on exercise-induced angina pectoris in patients with coronary artery disease.
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PMID:Effect of coffee on exercise-induced angina pectoris due to coronary artery disease in habitual coffee drinkers. 396 61

Slow responses were induced in rabbit isolated left atrial trabeculae in a modified Tyrode solution containing 15 mM-KCl and 1 mM-BaCl2. Conventional electrophysiological techniques were employed for stimulating and recording membrane potentials. Under these conditions, the excitability of the slow response depends on the past excitatory history of the preparation. As the stimulation frequency increases (range: 0.08-1 Hz) for a conditioning period of stimulation, the excitability of the slow response increases. This can be demonstrated by a decrease in stimulus requirement necessary to maintain slow response excitation following the conditioning period of stimulation. It is shown that when extracellular Ca2+ concentration is reduced to 0.5 mM, that phenomenon of frequency-dependent slow response excitability disappears but slow responses can still be elicited. Also, the addition of D-600 to 2.7 mM-Ca2+ solutions depresses both the slow response and its frequency-dependent excitability. The absence of frequency-dependent slow response excitability is not related to the depression of the slow response upstroke caused by low-Ca2+ solutions. Increasing intracellular Ca2+ concentration by exposing the preparation to low-Na+ solutions or to ouabain did not revert the observed effects in low-Ca2+ solutions. The addition of substances (5 mM-caffeine or 0.35 microM-adrenaline) that potentiate the influx of Ca2+ in low-Ca2+ solutions was found to be effective in restoring the dependence of slow response excitability on the frequency of stimulation. The increase in extracellular Ca2+ above 4 mM depressed the excitation of the slow response. Above 5.4 mM-Ca2+, the excitation of the slow response was completely inhibited while the preparation displayed continuous oscillations in transmembrane potential. The presence of a subthreshold response (subliminal response) that precedes and triggers slow response excitation is accompanied by tension development. Since the subliminal response is responsible for the changes in slow response excitability it is proposed that the Ca2+ inflow during slow response electrogenesis modulates the excitability of the slow response. Two possible physiological implications for this finding are discussed.
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PMID:Modulation of slow response excitability by calcium in rabbit atrial trabeculae. 402 Jul

It has been proposed that concomitant substances of abuse may have additive or synergistic properties such that alcoholics using other substances of abuse concurrently may have a harder time giving up alcohol than alcoholics abusing only alcohol. The present study surveyed 291 alcoholics in an alcohol treatment program and 86 social drinker controls matched on age, education, SES and gender. Alcohol consumption, smoking, coffee intake, other substances of abuse. Beck depression and Spielberger Anxiety (State) were measured. Alcoholics drank significantly more alcohol than did social drinkers per day (350.19 cc versus 28.08 cc, p less than 0.001), consumed more caffeine/day (486.3 mg versus 339.9 mg, p less than 0.002), smoked more cigarettes/day (27.8 versus 12.8, p less than 0.001), were more depressed (16.8 versus 4.4 (Beck), p less than 0.0001), had lower internal locus of control scores (37.6 versus 39.7, p less than 0.005), had higher scores on control by chance (22.7 versus 20.2, p less than 0.03) and were significantly more anxious (52.5 versus 33.9 on Spielberger's State Inventory p less than 0.0001). Some patients used stimulants, tranquilizers, depressants, narcotics or toluene. Only 3/258 abused alcohol without using other drugs. Results support earlier studies showing strong associations between alcohol and smoking and between alcohol and caffeine consumption. The alcoholic abusing only alcohol is very rare. Treatment programs need to pay attention to concomitant drugs of abuse.
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PMID:Treatment of alcoholism and concomitant drugs of abuse. 402 79

Studies have shown that adenosine analogs may modulate kindled seizures. The present study demonstrated that systemic administration of the adenosine analog, L-phenylisopropyladenosine (L-PIA), substantially prolonged the postictal depression and decreased the frequency of spiking that follows amygdala-kindled seizures in rats. Fully kindled rats were administered L-PIA (0.1 to 2.0 mg/kg, i.p.) or saline 30 min before stimulation of the amygdala. Afterdischarge durations with L-PIA did not differ from those with saline, and behavioral seizures were only slightly decreased in severity with 2.0 mg/kg L-PIA. However, 0.5 to 2.0 mg/kg L-PIA increased the duration of the postictal depression by more than 20 min and, at 2.0 mg/kg, L-PIA decreased the frequency of postictal spiking. Postictal administration of caffeine (32 mg/kg, i.p.) reversed the prolongation of the postictal depression induced by 1.0 mg/kg L-PIA. These effects did not seem to be mediated by peripheral actions of L-PIA (i.e., lowered blood pressure) as hydralazine, which decreases blood pressure through peripheral mechanisms, did not affect ictal or postictal events. These results indicate that adenosine may modulate neuronal excitability that follows kindled seizures.
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PMID:Prolonged postictal depression in amygdala-kindled rats by the adenosine analog, L-phenylisopropyladenosine. 406 71

Effects of caffeine on the action potential and contractile force of human atrial fibres obtained at cardiac surgery were studied with standard microelectrode technique. In 4 mmol . litre-1 [K]o, the only significant action produced by 0.3 to 3 mmol . litre-1 caffeine on the electro-mechanical activity of relatively normal atrial fibres was a slight shortening of the action potential duration at 50% repolarisation. When the fibres were depolarised in 27 mmol . litre-1 [K]o or in atrial fibres showing slow responses in 4 mmol . litre-1 [K]o, however, caffeine could increase the upstroke of slow response and the force. In 18% of atrial fibres showing slow responses in 4 mmol . litre-1 [K]o, caffeine induced spontaneous discharges and potentiated afterdepolarisations. The positive inotropic and the arrhythmogenic effects of caffeine could be diminished by pretreating the fibres with propranolol or Ca antagonists (diltiazem and verapamil). In fibres beating spontaneously in normal [K]o, caffeine accelerated spontaneous rhythms initially and then depressed them. Propranolol potentiated the later depression but did not block the initial acceleration. The results suggest that caffeine increases the transmembrane Ca influx and enhances the release of Ca from the intracellular stores in human atrial fibres. As a consequence, caffeine could induce arrhythmias in atria from certain individuals.
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PMID:Electromechanical effects of caffeine in isolated human atrial fibres. 408 29

1. Ouabain given by intracerebroventricular injection to mice in small doses (0.1-0.4 mug) produced a dose related depression of central nervous activity, characterized by a reduction in spontaneous locomotor activity, hypothermia, catalepsy and ptosis, lowered body posture and lack of response to external stimuli. Doses above 0.4 mug were excitatory, convulsant and lethal.2. The depressant effects could be antagonized by (+)-amphetamine, desmethylimipramine, dibutyryl cyclic 3'5'-adenosine monophosphate and caffeine.3. The MAO inhibitor nialamide produced only a small antagonism of ouabain, resulting in a greater rate of recovery from the depressant effects of ouabain.4. The depressant effects were associated with a marked elevation of whole-brain dopamine levels with little change in noradrenaline or 5-hydroxytryptamine.5. The dopamine-beta-hydroxylase inhibitor sodium diethyldithiocarbamate, administered by intracerebroventricular injection, produced effects qualitatively similar to those seen after ouabain.6. An interference with central transmitter function is postulated as a possible mode of action of intracerebroventricularly injected ouabain.
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PMID:Pharmacological properties of centrally administered ouabain and their modification by other drugs. 432 23

The in vitro transforming capacity of simian virus 40 (SV40) for Syrian hamster cells is highly resistant to inactivation by UV light in comparison to infectivity. In the same cell system, we demonstrated a "host cell repair mechanism" sensitive to caffeine which is, to a large extent, responsible for the high resistance to UV inactivation of the transforming capacity of SV40. The survival of infectivity of UV-irradiated SV40 in CV-1 cells was also sensitive to caffeine, again indicating host cell repair. On the other hand, depression of normal cell DNA synthesis by hydroxyurea during the first 24 h postinfection only modestly reduced, and to a similar extent, the transforming capacity of UV-irradiated and nonirradiated SV40.
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PMID:Analysis of minimal functions of simian virus 40. 3. Evidence for "host cell repair" of oncogenicity and infectivity of UV-irradiated simian virus 40. 435 29

1. In the neuronally isolated cortex of the cat, local application of bemegride, picrotoxin, nikethamide, caffeine and strychnine facilitated the surface positive response of the isolated cortex and lowered the stimulus threshold for this response. Excepting nikethamide, they all produced convulsive discharge in the isolated cortex unrelated to the applied stimulus.2. Local application of glutamate to the cortex produced spreading depression, which was sometimes preceded by spontaneous positive bursting.3. In contrast to the "general depressants" which produce a relatively consistent pattern of effects on the electrical responses of isolated cortex, the "general stimulants", although they all have excitatory effects on isolated cortex, each produced a greatly different type of electrical response in the isolated cortex, suggesting that several different mechanisms of action are responsible for their effects.
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PMID:Effects of general stimulant drugs on the electrical responses of isolated slabs of cat's cerebral cortex. 439 70


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