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)

Investigations of the fine structural changes observed in the hearts of cardiomyopathic hamsters at very early stages of the disease indicate that the initial changes involve the pericapillary mesenchymal cells. Other prominent features consist of hypercontraction of cardiocytes, disruption of intercalated disks, and eventual partitioning of cardiac cells, with myofibrillar lysis. The generalized plasma membrane defect allows a net increase in calcium influx and a depression in mitochondrial respiratory control ratios. These pathologic events are in accord with previously reported increases in myocardial sympathic nerve activity.
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PMID:Cardiomyopathy of hamster dystrophy. 28 24

1. The time course for the changes in miniature end-plate potential (min epp) frequency and in epp amplitude produced by alterations in the tonicity of the Ringer at the frog neuromuscular junction was studied. The relations between the tonicity and min epp frequency as well as epp amplitude were also investigated. 2. The change in min epp frequency occurred within 1 min after the start of the change in the tonicity of the extracellular solution. Following a shift to a hypertonic solution, the min epp frequencies were often maintained at a relatively steady, elevated level, even with large (+100 mosM) changes in tonicity. In other instances the elevation was transitory like the reported data for the rat neuromuscular junction. Essentially the same results were obtained in very low Ca2+-Ringer. Unlike the rat neuromuscular junction, the final level after hours of the increased min epp frequency caused by raising the osmolarity by more than 75 mosM was well above the control level. Following the return from a hypertonic to an initial solution there was a prompt decrease in min epp frequency to about the initial level; there was no indication of the transitory depression in min epp frequency following the return from hypertonic solution that has been reported in mammals. 3. Until the osmolarity of the Ringer reached about 420 mosM, the frequency of min epp continued to rise along a line relating log (min epp frequency) to (osmolarity)0.5. When the osmolarity exceeded 460 mosM, the relation started to level off. 4. The hypothesis that the min epp frequency in a Ringer with a given increased tonicity is a fixed multiple of the frequency in normal Ringer is not in accord with the data. 5. The decrease in epp amplitude caused by markedly hypertonic solutions also came about within 1 or 2 min after the start of the change in the tonicity of the solution surrounding the nerve terminal. 6. Hypertonic solutions did not appear to affect facilitation. 7. Below 360 mosM increasing the tonicity of the Ringer had little effect on the amplitude of epp. Above this level the amplitude decreased as the tonicity increased. At a given junction an increase in tonicity in a range above 360 mosM can cause an increase in min epp frequency and a decrease in epp amplitude. 8. The results are discussed in terms of the theories proposed to account for the effects of osmolarity on synaptic function. Two theories--the water flow hypothesis (11) and the barrier of water hypothesis (2)--do not fit with the results. The two other theories--calcium elevation (1) and screening of surface charges (3, 13, 21)--fail to account for important aspects of the results and therfore cannot be accepted without substantial modifications. None of the theories devised to account for the increase in min epp frequency predicts the falloff in frequency and in evoked quantal release that occurs in highly hypertonic solutions.
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PMID:Time course and magnitude of effects of changes in tonicity on acetylcholine release at frog neuromuscular junction. 30 Apr 28

The influences of octanoic, decanoic, and hexadencanoic acid were tested on the contracture capability of isolated skeletal muscle of frogs and rats. 1. 100 mM octanoic or 10mM decanoic acid induce contractures in skeletal mucles after 20-30 min of exposure. 2. The time of exposure necessary for induction of contractures is shortened by an increase of bath temperature, electrical stimulation or KCl-depolarization of muscles. 3. Simultaneous addition of fatty acid and caffeine (10 mM) effects a depression and a delay of the caffeine contracture. The contractures evoked by 5 mM caffeine are inhibited by lower concentrations of fatty acids (1 mM octaonoic acid, 0,1 mM hexadecanoic acid). 4. After the complete development of a caffeine (or fatty acid) contracture the muscle is not able to develop an identical contracture by a second application of the same drug, even after intermediate treatment during one or two hours in Ringer solution. If the contracture is interrupted one minute after the caffeine application by changing the solution, the tension returns quickly to the resting level. A subsequent addition of caffeine (10 mM) after about 10 minutes effects an identical contracture. Thus the effect of fatty acids on caffeine contracture may be studied on the same muscle which served as its own control. 5. As mechanisms involved in the development of fatty acid contractures and in the inhibition of caffeine contractures, interactions of free fatty acids and lipids of biological membranes are disucssed. Especially, there may be changes of the calcium affinity of cellular membranes.
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PMID:[Influence of homologous n-alcanoic acids on the function properties of isolated skeletal muscles. III. Contractures by fatty acids and relations to the effects of caffeine]. 30 81

1. When motor nerve terminals are slightly depolarized with increased [K+]o, progressive increases in [Ca2+]o raise min.e.p.p. frequencies until a maximum is reached; further increases then produce a depression (Cook & Quastel, 1973; Matthews & Wickelgren, 1977). 2. Increases in [Mg2+]o also produce the depression. 3. It has been suggested that the depression results from this sequence of events: (a) the divalent cations screen the fixed negative surface charges on the outer face of the nerve terminal, which (b) decreases the negativity of the surface potential, which (c) increases the voltage gradient within the membrane itself, which (d) tends to shut depolarization-gated channels for Ca2+ entry, which (e) decreases min.e.p.p. frequency. 4. In agreement with the interpretation, in frog neuromuscular junctions slightly depolarized with 11 mM-[K+]o, min.e.p.p. frequency is a monotonically increasing function of [Ca2+]o, as long as the sum of [Ca2+]o plus [Mg2+]o is kept constant. 5. The decrease in min.e.p.p. frequency caused by raising [Mg2+]o by 5 mM can be counterbalanced by raising [K+]o by about 9 mM. Using the Grahame equation (1947), assuming that the elevated divalent cations act solely by screening and have no effect on conductance, the negative surface charge is estimated to be roughly 1 electronic charge/75 A2.
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PMID:Surface charges and the effects of calcium on the frequency of miniature end-plate potentials at the frog neuromuscular junction. 30 31

The effects of the ionophores A-23187 and X-537 A on glucose metabolism, ATP content and sucrose permeability in pancreatic islets microdissected from obese-hyperglycemic mice were studied. The formation of 14CO2 from 10 mM D-[U-14C] GLUCOSE WAS INHIBITED BY OMISSION OF Ca2+ from the medium. A-23187 (10 muM) induced a further decrease of 14CO2 formation whereas X-537 A (10 muM) had no effect. At 20 mM glucose both A-23187 (48 muM) and X-537 A (43 muM) decreased the 14CO2 formation in the absence of Ca2+ whereas only X-537 A inhibited in the presence of Ca2+. X-537 A (43 muM) also decreased the formation of 3H2O from 20 mM D-[5-3H] glucose. The islet content of ATP was not changed after incubation in media deficient in either Mg2+ or Ca2+. However, omission of both Mg2+ and Ca2+ resulted in about 50% decrease of the ATP content. A-23187 and X-537 A induced dose-dependent decreases of the islet ATP content. X-537 A was much more potent than A-23187. Both ionophores induced stronger depression of the ATP content when Ca2+ was omitted. X-537 A (43 muM) but not A-23187 (48 muM) increased the beta-cell membrane permeability as indicated by an increased sucrose space in relation to the urea space of islets. Such an effect was not obtained with X-537 A at 1 muM or by omission of Ca2+. It is suggested that the marked metabolic effects of the ionophores reflect an impaired mitochondrial metabolism. These metabolic changes should be considered in interpretations of ionophore action on insulin secretion.
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PMID:Metabolic characteristics of pancreatic beta-cells exposed to calcium-transporting ionophores. 31 39

Increasing levels of magnesium were found to cause a marked depression of glucosestimulated insulin secretion at fixed calcium levels, particularly at levels which bracketed the concentration of ultrafiltrable magnesium found in normal rat plasma (1.3 meq/l), i.e., increasing magnesium from 0.6 to 1.2 meq/l depressed secretion, and increasing magnesium from 1.2 to 2.4 meq/l resulted in a further depression. Paradoxically, when magnesium was omitted from the perfusing medium, insulin secretion was also depressed. The data strongly suggest that the calcium/magnesium ratio is a primary regulator of the insulin secretory process, since a relatively slight alteration of the physiologic ratio of calcium to magnesium (approximately 2.5) results in a marked alteration of total insulin secretion. In addition, small amounts of magnesium are necessary for optimum secretion, possibly reflecting the requirement for magnesium in several enzymatic processes. Thus, magnesium may play an important role in the regulation of insulin secretion by altering the sensitivity of the beta cells of the Islets of Langerhans to glucose.
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PMID:Magnesium modulation of glucose-induced insulin secretion by the perfused rat pancreas. 32 55

Using a 2-hour 47Ca absorption test, significant depression of active calcium absorption was demonstrated in 48 vitamin D untreated haemodialysis patients. This malabsorption of calcium could be corrected by the daily oral administration of 1--2 microgram of 1alphaOHD3 and 1--1.5 microgram of 1,25(OH)2D3. 5 microgram daily for 2 weeks of 3-deoxy-1alphaOHD3 AND 16 and 64 microgram daily for 1 week of 24R,25(OH)2D3 proved ineffective. In 32 successfully transplanted patients, restoration of normal or near normal renal function (serum creatinine less than 1.9 mg/100 ml) was not always followed by an immediate improvement in active calcium absorption. Calcium absorption, especially in female patients, was adversely affected by the required immunosuppressive prednisone therapy and improvement was slow.
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PMID:Effect of 1alpha-hydroxycholecalciferol, 1,25-dihydroxycholecalciferol, 3 deoxy-1alpha-hydroxycholecalciferol, 24R, 25-dihydroxycholecalciferol and successful renal transplantation on calcium absorption in haemodialysis patients. 34 40

A therapeutic trial with verapamil, a calcium-antagonist drug, was performed in 12 patients admitted to our coronary care unit because of frequent daily attacks of angina at rest attributed to coronary vasospasm. After a 48-hour run-in period, oral verapamil 480 mg/day and placebo were administered alternately during 4 randomised 48-hour periods. Transient ischaemic attacks with ST segment elevation or depression, with or without pain, were documented by continuous electrocardiographic monitoring. The number of attacks during the run-in and 2 placebo periods were 128, 123, and 130, respectively, and 31 and 23 during the 2 treatment periods (P less than 0.006 and P less than 0.003). This drug therefore appears to be effective in the management of patients with frequent attacks of angina at rest.
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PMID:Management of unstable angina at rest by verapamil. A double-blind cross-over study in coronary care unit. 37 44

1. A study has been made of the effects of changing the external calcium concentration [Ca](o) on the binomial parameters p and n that control the average quantal content (m) of the end-plate potential (e.p.p.) during trains of nerve impulses at synapses in amphibian striated muscle.2. In high external calcium concentrations (0.4 mM </= [Ca](o) < 1.0 mM) the increase in m of a test impulse following a conditioning impulse at different intervals (< 100 msec) was due to an increase in the number of quanta available for release, n; the increase in m of successive e.p.p.s in a short high frequency train was primarily due to an increase in n.3. In high external calcium concentrations (1.0 mM </= [Ca](o) < 10 mM) there was a decrease in m of a test impulse following a short high frequency conditioning train (4-5 impulses, 20-100 Hz) at different intervals (200 msec < 5 sec) and this was due to a decrease in the number of quanta available for release, n; in a long high frequency train (20 impulses, 20-100 Hz) there was an increase in m for the first few successive e.p.p.s followed by a depression of m which eventually reached a steady state and these changes in m were due to changes in n; the higher the frequency the greater was the depression in n during the steady-state period.4. In high calcium concentrations, the steady-state m reached in the first 20 impulses during continual stimulation at high frequency gave way to a decline in m over several minutes until a new depressed steady-state value of m was reached and this was maintained during the longest periods of stimulation (30 min); this decline in m was primarily due to a decline in the number of quanta available for release.5. These changes in the number of quanta available for release during trains of impulses are predicted in terms of a hypothesis in which facilitation is due to the accumulation of a residual calcium-receptor complex in the nerve terminal that determines the fraction of a pool of quanta which contributes to n, and depression is due to a decrease in the number of quanta in this pool.
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PMID:The effects of calcium ions on the binomial parameters that control acetylcholine release during trains of nerve impulses at amphibian neuromuscular synapses. 41 20

In a group of ten male adults admitted to hospital with clinical symptoms of lead exposure, phenazone, elimination rates, blood delta-amino-laevulinic acid dehydratase (ALA.D) activity, blood lead levels and haemoglobin were measured. Investigations were carried out before, immediately after and again at least 12 weeks after cessation of CaEDTA (sodium calcium edetate) chelation therapy. Following chelation, phenazone elimination rates were increased as assessed by a decrease in half life and increase in clearance. This was significant, both immediately after and 12 weeks after cessation of chelation therapy. The change in rate of phenazone metabolism was associated with improved clinical status, with lowered blood lead levels and raised haemoglobin and ALA.D activity. The results of the study suggest that the depression in phenazone elimination in lead intoxication is possibly due to depressed hepatic cytochrome P450 levels.
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PMID:The effects of industrial lead poisoning on cytochrome P450 mediated phenazone (antipyrine) hydroxylation. 41 77


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