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)

Muscarinic, cholinergic depression of adrenergic excitatory transmission was investigated by the microelectrode method in isolated dog retractor penis muscle. Electrical stimulation of the intramural nerves with single or repetitive stimuli elicited adrenergic contractions and excitatory junction potentials (e.j.p.s). The mechanical response and e.j.p. were suppressed by physostigmine (5 x 10(-7) g/ml) and carbachol (up to 5 x 10(-8) g/ml) without changing the sensitivity of the muscle to noradrenaline and muscle membrane resistance measured by electrotonic potentials. Atropine reversed the drug-induced attenuation of these responses, but atropine itself had no effect on them. Carbachol at 5 x 10(-8) g/ml, where the e.j.p. was blocked, caused a depolarization of the muscle membrane (less than 5 mV), whereas the same extent of depolarization produced by high K solution resulted in only a small decrease in e.j.p. amplitude. These results suggest that excitatory adrenergic transmission in the dog retractor penis muscle is depressed prejunctionally by a cholinergic mechanism.
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PMID:Cholinergic inhibition of adrenergic transmission in the dog retractor penis muscle. 632 83

The effects of atropine and glycopyrronium, when given intravenously with neostigmine during the reversal of neuromuscular blockade in patients with cardiovascular disease, were compared in a double blind trial. Atropine was associated with a significantly greater elevation of heart rate and rate-pressure product than glycopyrronium. This elevation was also more sustained with atropine. The entire atropine population also showed a significantly greater incidence of ST-segment depression on the electrocardiogram than that observed in those who had received glycopyrronium. Furthermore, patients with ischaemic heart disease and previous myocardial infarction who received atropine showed a significantly greater incidence of dysrhythmias than those given glycopyrronium. It is suggested that at the time of reversal of neuromuscular blockade in patients with cardiovascular disease, glycopyrronium is a more suitable agent than atropine.
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PMID:Comparison of atropine and glycopyrronium in patients with pre-existing cardiac disease. 651 48

Clonidine (10(-9)-3 X 10(-6) M) produced a concentration dependent inhibition of field stimulation-induced contractions of rat detrusor muscle strip at 0.1 and 1 Hz which were completely abolished by tetrodotoxin (5 X 10(-7) M) but were unaffected by hexamethonium (10(-5) M). Pretreatment with yohimbine (10(-8)-10(-7) M) did not modify the amplitude of contractions but produced a rightward parallel shift of clonidine's cumulative response curve without a depression of the maximal response. The corresponding pA2 value for yohimbine was 8.44 +/- 0.1. Atropine (3 X 10(-6) M) produced a partial inhibition of contractions at both frequencies. In the presence of atropine the cumulative response curve of clonidine was significantly reduced at 1 but not at 0.1 Hz. Indomethacin (5 X 10(-5) M) and theophylline (2 X 10(-4) M) produced a partial inhibition of amplitude of contractions at both frequencies without any interference with the effect of a supramaximal concentration of clonidine. Prazosin (10(-6) M), propranolol (10(-6) M), chlorpheniramine (10(-6) M), ranitidine (10(-6) M), haloperidol (10(-7) M), pizotifen (10(-6) M), naloxone (10(-6) M), quinidine (10(-6) M), strychnine (10(-5) M) or picrotoxin (10(-5) M) neither affected the amplitude of contractions at either frequency nor antagonized clonidine effects. The contractile response of non stimulated strips to acetylcholine (10(-5) M), carbachol (3 X 10(-6) M) and ATP (10(-3) M) were not significantly influenced by pretreatment with clonidine (3 X 10(-6) M). These results suggest that stimulation of prejunctional alpha 2-adrenoreceptors located on postganglionic nerve endings might reduce the output of excitatory neurotransmitter(s) in rat urinary bladder.
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PMID:The effects of clonidine on electrically-induced contractions of rat detrusor strips in vitro. 664 49

Cutaneous pectoris muscles of Rana pipiens were transected distal to the innervated region. Within 10 min, membrane potentials (Em's) of -33 +/- 2.5 mV and end-plate potentials (3-15 mV) were recorded unaccompanied by muscle action potentials or twitch. The fall in Em was associated with a net loss of [K+]i and a net gain of [Na+]i. Although input resistance fell by 50% and the space constant was slightly reduced in the transected muscle fibers, end-plates could be adequately voltage-clamped with two microelectrodes. End-plate currents (e.p.c.s) with rise times of 350 to 700 musec were recorded as a function of holding potential (Vm). The current-voltage relationship of peak e.p.c.s over the range of -70 to +20 mV was linear and the reversal potential (-6.6 +/- 2.2 mV) was the same as that found for intact muscle fibers. The decay phase of e.p.c.s could be described as a single exponential at all Vm's and had a voltage and temperature dependence similar to that described for e.p.c.s of glycerol-treated muscles. Tubocurarine (0.3 microM) caused a significant decrease in the time constant (tau) of e.p.c. decay and e.p.c. amplitude. The depression of e.p.c. amplitude by tubocurarine was reversed by 4-aminopyridine while the decrease of tau was not. Atropine (10(-4) M) caused a monotonic shortening of e.p.c.s at a Vm of -90 mV but e.p.c.s recorded at +50 mV were biphasic. Lidocaine, a quaternary nitrogen analog of lidocaine (QX314), lobeline and hexafluorenium were studied also in transected muscle and their effects on the parameters of e.p.c. are described. Both lobeline (50 microM) and hexafluorenium caused a decrease of tau and eliminated the voltage dependence of tau at negative Vm's. The transected muscle can be used for the study of conductance kinetics of end-plate and for the study of drug action uncomplicated by the presence of other drugs of Mg++ to eliminate contraction.
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PMID:Characterization of end-plate conductance in transected frog muscle: modification by drugs. 696 98

Clonidine poisoning usually causes depressed sensorium, hypotension, and bradycardia. Some patients manifest respiratory depression and miosis simulating narcotic overdose. Supportive care with judicious administration of intravenous fluids, occasionally supplemented by a dopamine infusion, usually reestablished adequate blood pressure. Tolazoline, an alpha-blocker, may reverse clonidine's effects should other efforts fail. Atropine should be used if bradycardia is hemodynamically significant. With massive overdose, clonidine's partial alpha-agonist properties may predominate, resulting in marked hypertension requiring cautious therapy. The experience at Parkland Memorial Hospital with clonidine overdose in six patients demonstrates the myriad of clinical presentations possible.
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PMID:Clonidine overdose: report of six cases and review of the literature. 701 72

1. The myenteric plexus-longitudinal muscle preparation of the guinea-pig ileum was incubated with [(3)H]choline (1.125-1.5 muM), and then superfused with Tyrode solution containing hemicholinium-3 (10 muM). Secretion of [(3)H]acetylcholine ([(3)H]ACh) was evoked either (a) by electrical field stimulation (0.5-15 Hz, 150 shocks per period, 0.5 msec), used to ;indirectly' depolarize the varicosities of nerve terminals, or (b) by high potassium (40 mM with 1 muM-tetrodotoxin, for 6 min, or 80 mM without tetrodotoxin, for 1 min), to ;directly' depolarize varicosities.2. With these stimulation parameters, which yielded about the same fractional secretion of [(3)H]ACh, and with eserine (10 muM) present in the medium, atropine (1 muM) enhanced the ;indirectly', electrically evoked secretion 3.65+/-0.34 (n = 6) fold, and that caused by 40 mM or 80 mM-potassium 1.82+/-0.06 (n = 6) or 1.55+/-0.09 (n = 10) fold, respectively. Atropine thus enhanced ;indirectly', electrically evoked secretion 4-fold more than that caused by ;direct' depolarization of varicosities with high potassium (P < 0.001).3. This difference is not likely to be caused by depression of the sensitivity of the presynaptic muscarinic receptors to ACh released by nerve stimulation, caused by the hypertonicity of the medium in the potassium stimulation experiments. The medium made hypertonic by addition of Tris-HEPES (80 mM) did lower the binding affinity of membrane preparations of (pre- and post-synaptic) muscarinic receptors, to carbamylcholine, and also the contractile responsiveness of the longitudinal muscle to this agent, in both cases to about one half. But it did not appear to alter the responsiveness of either pre- or post-synaptic muscarinic receptors to endogenous ACh, released by nerve stimulation.4. The results support a dual-mode model for the muscarinic negative feed-back control of ACh secretion from the nerve terminals of this preparation, mainly operating by restriction of the invasion of terminals, and only secondarily by depression of the efficiency of depolarization-secretion coupling in invaded varicosities.5. Since this model has earlier been proposed to apply for the control of secretion of [(3)H]noradrenaline from the micro-anatomically similar nerve terminals of noradrenergic nerves, the present findings suggest that the model may have a wider biological significance, and possibly apply to the control of the secretory activity of boutons-en-passant nerve terminals in general.
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PMID:The effects of atropine on [3H]acetylcholine secretion from guinea-pig myenteric plexus evoked electrically or by high potassium. 714 61

Cardiovascular adjustments induced by topical application of drugs on a restricted area on the ventral surface of the medulla oblongata, corresponding to the caudal part of the rostral chemoreceptor area and the intermediate area, have been studied in chloralose-anesthetized cats. Topical application of GABA or glycine on these structures resulted in blood pressure fall, bradycardia, vasodilatation in the kidney and the skeletal muscles and also depression of respiration. Similar responses except for a slight tachycardia occurred with application of physostigmine. Application of GABA resulted in a marked attenuation of the reflex vasoconstrictor responses to removal of arterial baroreceptor restraint (carotid occlusion), particularly in the kidney, and to disappearance of the reflex renal vasodilatation to baroreceptor stimulation. The findings suggest that GABA application leads to a general diminution of the tonic vasomotor neuron activity, and with regard to renal vasomotor neurons a virtual cessation. Atropine methylnitrate application induced blood pressure rise, increased peripheral resistance in both skeletal muscle and kidney and a strongly potentiated renal vasoconstrictor response to carotid occlusion. The results indicate that the studied superficial medullary structures play an important role for the maintenance of tonic vasomotor neuron activity, especially renal.
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PMID:Cardiovascular effects elicited from the ventral surface of medulla oblongata in the cat. 719 82

The activity of a selective cholecystokinin (CCK)-A receptor agonist, N-acetyl derivative of A71623 (Ac-Trp-Lys(epsilon-N-[2-methylphenylamino-carbonyl]) -Asp-(NMe)Phe-NH2) was investigated in the guinea pig isolated ileum longitudinal muscle myenteric plexus. NAA caused both a phasic and tonic contraction at all concentrations tested (1-1000 nM). The selective CCK-A antagonist L-364,718 (Devazepide) antagonized both types of contraction with a pKB of 10.10 and 9.95, respectively. The CCK-B selective antagonist L-365,260 ((3R(+)-2,3-dihydro-1-methyl-2-oxo-5-phenyl-1H-1, 4-benzodiazepine-3yl)-N-(3-methylphenyl)-urea) was inactive up to a concentration of 30 nM. Atropine at 300 nM and 1000 nM reduced the maximal response of NAA by only 17% and 50%, respectively. The selective neurokinin (NK)-1 antagonists GR 82334 ([D-pro9[Spiro-gamma-Lactam] Leu10, Trp11]-Phys (1-11)9) at 300 and 1000 nM and (+-) CP-96,345 [(2S, 3S)-cis- 2-(diphenylmethyl)-N- [(2-methoxyphenyl)-methyl] -1-azabici-clo [2.2.2]octan-3-amine] at 10 nM were inactive or partially active. When atropine and GR 82334 or (+/-) CP-96,345 were combined, they produced a dose-dependent synergistic inhibition of both phasic and tonic contractions induced by NAA. The selective NK-3 receptor agonist senktide induced both phasic and tonic contractions that were blocked by tetrodotoxin. In the presence of atropine and GR 82334, both 300 nM, a synergistic depression of the response to senktide similar to that observed for the agonist NAA was disclosed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A further analysis of the contraction induced by activation of cholecystokinin A receptors in guinea pig isolated ileum longitudinal muscle-myenteric plexus. 752 Sep 41

The paper presents the results of electrophysiological studies of the function of the sinus node, sinoatrial and atrioventricular conduction in 62 patients with acute clofelin poisoning and of drug correction of the said disorders. Atropine, asthmopent, dobutrex, and butyroxan were used. Toxicogenic depression of the sinus node and conduction disorders in the sinoatrial zone and atrioventricular junction were detected, with blocking of the entrance and exit or isolated blocking of the exit forming in the sinoatrial zone in some patients. All the drugs used improved the conduction in the sinoatrial zone and atrioventricular junction.
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PMID:[Variants of drug treatment of disorders of the conductivity in the sinoatrial zone and atrioventricular junction in patients with acute clofelin poisoning]. 765 72

1. The responses of bladder strips from control, streptozotocin-diabetic, and sucrose-drinking rats to electrical field stimulation were investigated. Sucrose-drinking rats were included as additional controls because they have enlarged bladders as a result of non-diabetic diuresis. 2. Bladder strips from diabetic rats developed more spontaneous activity than those from the two control groups. Indomethacin reduced the amplitude and frequency of spontaneous contractions suggesting that they resulted from endogenous prostaglandin formation. Tetrodotoxin (TTX) had little effect, while alpha, beta-methylene ATP caused increases in spontaneous activity. 3. Bladder strips from diabetic rats responded to field stimulation with greater contractions than controls in the absence of antagonists as well as in the presence of atropine and alpha, beta-methylene ATP. Increasing TTX concentrations caused a step-wise depression of the contractile response to electrical stimulation which was not affected by preincubation with either atropine or alpha, beta-methylene ATP. 4. Atropine and indomethacin had no effect on strength-duration curves constructed to measure threshold contractile responses to five pulses stimulation. The curves were shifted to the right by both TTX and alpha, beta-methylene ATP, indicating that the responses were neurogenic in nature and at least partially, the result of stimulation of P2-purinoceptors. In the absence of drugs, bladder strips from diabetics responded at lower voltages and pulse widths than those of control and sucrose-drinking rats, suggesting that they were more excitable. 5. The response curve of bladder strips from diabetics to field stimulation at increasing voltage was shifted upwards and to the left compared to strips from control or sucrose-drinking rats. 6. Bladder strips from diabetics responded to stimulation at increasing pulse width with greater responses than those from control or sucrose-drinking rats. At 1.0 ms pulse width, the TTX-resistant response of strips from diabetic rats was still greater than that of the other groups, indicating that a myogenic component was also involved.7. The data suggest that bladder strips from diabetic rats are more excitable than those of control or sucrose-drinking rats. This may result from diabetes-induced decreases in bladder lipid or other membrane changes, and/or be a result of partial depolarization, perhaps related to diabetic neuropathy.
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PMID:Factors underlying the increased sensitivity to field stimulation of urinary bladder strips from streptozotocin-induced diabetic rats. 781 10


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