UMLS:C0011570 - FACTA Search

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Query: UMLS:C0011570 (depression)
172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chlorpromazine (ClP) and trifluoperazine (TFP) depress electrical and mechanical activity of ureter smooth muscle cells. Contraction was depressed by less doses of the substances applied as compared with the processes responsible for generation of spike activity. ClP causes the displacement of the dose-effect curve for Ca2+ towards larger concentrations of the latter. Trifluoperazine displaces the dose-effect curve for contraction to the right and downwards. It is concluded that inhibition of contraction and depression of ClP and TFP spikes is due to the calmodulin blocking on which kinase activity of myosin light chains depends. It is supposed that processes responsible for activation of the membrane systems of Ca2+ transport in the process of spike generation are also calmodulin-dependent.
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PMID:[Study of electromechanical coupling in smooth muscle cells of the ureter using phenothiazines]. 672 4

The effect of shortening during activity, previously characterized in vertebrate striated muscle, was investigated in the anterior byssus retractor muscle (ABRM) of the mollusc Mytilus edulis. This muscle is considered to have an essentially myosin-linked Ca2+-regulatory system. Release steps of different amplitude were performed during isometric phasic contraction, and force redevelopment was recorded at a muscle length L1, defined as 90% of the muscle length at which a slight resting tension, approximately 1 mN, appeared in the presence of 2.5 X 10(-5) M 5-HT. Active shortening caused a graded depression of the contractile force without affecting the total duration of the mechanical response. Peak redeveloped force after muscle shortening of 0.06 L1 and 0.18 L1 was reduced by approximately 1.5% and 7.0%, respectively, of the isometric tension value at L1. The shortening effect was fully reversible, and had a lifetime of approximately 8 to 9 s. The depressant effect of active shortening was augmented at a reduced degree of activation of the muscle. The presence of caffeine and dantrolene and altered tonicity of the extracellular medium (0.9 T-1.2 T) did not significantly affect the shortening induced depression obtained at maximum phasic activation of the preparation. The nature of the shortening effect is compared to that obtained in vertebrate striated muscle and is discussed on the basis of differences in Ca2+-regulation of the contractile system in these two muscles.
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PMID:Depressant effect of active shortening in the anterior byssus retractor muscle of Mytilus edulis. 688 Jul 96

Nerves to fast- and slow-twitch cat muscles were stimulated with various numbers of supramaximal pulses under isometric conditions. By subtracting the force produced by j - 1 pulses from that produced by j pulses, the contribution of the j th pulse could be compared with the response to one pulse (twitch response). A less-than-linear summation (depression) was observed during the rising phase of the twitch. This depression became increasingly prominent and longer in duration with repetitive stimulation. A more-than-linear summation (facilitation) was observed during the falling phase of the twitch, which became increasingly delayed and smaller in amplitude with repetitive stimulation. The early depression could be abolished for the first few pulses by Dantrolene [1-(5-p-nitrophenyl) furfurilidene amino hydantoin sodium hydrate], which reduced Ca++ release from the sarcoplasmic reticulum. The depression was less prominent at short muscle lengths or with stimulation of single motor units. A first-order, saturable reaction such as Ca++ binding to troponin or actin binding to myosin can quantitatively account for the early depression.
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PMID:Nonlinear summation of contractions in cat muscles. I. Early depression. 732 3

1. The goal of this study was to characterize the fatigability, contractile relaxation properties, electrophysiological responses, and histochemical properties of the human paralyzed soleus muscle to determine its relative plasticity. 2. Acute (< 6 wk, n = 3) and chronic (> 1 yr, n = 10) paralyzed individuals had the tibial nerve activated with a 20-Hz square wave delivered for 330 ms every second for 4 min. The soleus muscle peak torque, one-half relaxation time (1/2RT), normalized maximum rate of relaxation (nMRR), and mass muscle action-potential amplitude (M wave) were computed every 30 s. A soleus muscle biopsy was evaluated for myosin adenosine triphosphatase enzyme (ATPase; pH 9.4, 4.6, and 4.2) and nicotinamide adenine dinucleotide tetrazolium reductase (NADH-TR). 3. In the chronically paralyzed group the torque was significantly reduced within 30 s of the fatigue protocol. The 1/2RT and nMRR were also significantly changed within 30 s, supporting that muscle relaxation was prolonged. No significant changes were present at comparable times during the same 4-min fatigue protocol applied to the acutely paralyzed soleus muscle. M-wave amplitude was significantly reduced in the chronic group, but only at 3 min of the fatigue protocol. Conversely, no significant changes occurred to the M waves of the acute group. 4. The correlation was high between torque and nMRR (r = 0.88-0.97) and torque and 1/2RT (r = 0.88-0.96) for each chronic subject. A close association was also found between 1/2RT and nMRR (r = 0.88-0.92) for each chronic subject. Because these variables changed minimally in the acutely paralyzed group, a lower correlation was present (r = 0.45-0.52). 5. Torque was weakly correlated to M-wave amplitude (r = 0.55) for the chronically paralyzed group. The greatest change in torque occurred at a time (0-65 s) when the least amount of change occurred in the M-wave amplitude, suggesting that the source of fatigue was within the contractile mechanism and not attributable to neuromuscular transmission compromise. 6. Despite a close association between torque and relaxation properties during fatigue of the chronically paralyzed soleus muscle, there was a significant dissociation after 5 min of recovery. Torque recovered to 60%, whereas the relaxation properties were consistently fully recovered. This suggests that the mechanism causing torque reduction covaried with the mechanism leading to prolonged relaxation during fatigue, but during recovery the two mechanisms no longer covaried. M-wave amplitude was also completely recovered at 5 min despite continued torque depression.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Fatigability, relaxation properties, and electromyographic responses of the human paralyzed soleus muscle. 766 32

Superior cervical ganglion neurons (SCGNs) were isolated from 7-day-old rat SCG and cultured in MEM containing horse serum, fetal calf serum, and nerve growth factor. In this culture condition, it is well known that the SCGNs form cholinergic synapse. In 3-4 weeks cultured neurons, immunofluorescent staining for synaptophysin, a small synaptic vesicle associated protein, showed the presence of synaptophysin as small dots on the surface of the soma. Postsynaptic potentials could be recorded in 50-80% of the neurons responding to evoked action potentials elicited in neighboring neurons. Because of its relatively large cell size and the short distance to the terminal, this synapse is a useful model for studying the mechanisms of acetylcholine (ACh) release by introducing substances such as antibodies or selective inhibitors into the presynaptic neuron by means of the whole-cell clamp technique. In this model synapse we tested the possible role of myosin in ACh release. The distribution of myosin was studied by the immunofluorescent staining technique. Myosin was recognized by the anti-myosin II IgG at the same synaptic terminals that showed the presence of synaptophysin with its antibody. The functional blockade of myosin by the antibody itself, and that of myosin light chain kinase (MLCK) by a pseudosubstrate inhibitor of MLCK, SM-1, or by a selective inhibitor of MLCK, wortmannin, induced depression of synaptic transmission in a dose-dependent manner. These indicate that phosphorylation of myosin by MLCK may be necessary for ACh release mechanisms.
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PMID:Analysis of the mechanism for acetylcholine release at the synapse formed between rat sympathetic neurons in culture. 781 40

Hypertrophy of isolated adult feline cardiac muscle cells may be induced in culture by either alpha- or beta-adrenergic agonists. However, it has been shown previously that each of these agonists activate different subsets of immediate-early response genes and have different effects on expression of "fetal" protein isoforms and stimulation of protein synthesis. Moreover, in adult feline heart cells, beta-adrenergic agonists, such as isoproterenol, activate sustained synchronous beating and sarcomeric reorganization while alpha-adrenergic agonists, such as phenylephrine, do not. The objective of the present study was to determine whether these differences in proximal signaling events converged in a common signal pathway during activation of contractile protein synthesis. By direct comparisons of actin and myosin heavy chain (HC) synthesis and accumulation following isoproterenol and phenylephrine, it was determined that both agonists stimulate a coordinated accumulation of these proteins during cardiomyocyte growth. However, each agonist stimulated a very different program of contractile protein synthesis. During phenylephrine-induced hypertrophy, actin and myosin HC syntheses were rapidly and coordinately activated and continuously maintained at rates 10-25% greater than untreated cultures. The pattern of myosin HC synthesis following isoproterenol was very much more complex with periods during which it was as much as 40% greater or 25% less than in control cultures. Furthermore, there was no correlation between rates of actin and myosin HC synthesis following isoproterenol. It was concluded that actin and myosin HC syntheses and accumulation were regulated independently and in a very different manner following isoproterenol or phenylephrine. Since protein accumulation was not correlated with synthesis rates during development of hypertrophy, it was also concluded that post-translational mechanisms played a significant role in the maintenance of contractile protein stoichiometry during beta-adrenergic/beating-induced hypertrophy. Myosin HC synthesis also appeared to be independently regulated during cardiomyocyte atrophy induced by the calcium channel blocker nifedipine. Unlike the case in hypertrophy, however, protein balance was not maintained in nifedipine, and the depression of myosin HC synthesis and loss of myosin HC content were much greater than in the case of other contractile proteins.
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PMID:Myosin heavy chain synthesis is independently regulated in hypertrophy and atrophy of isolated adult cardiac myocytes. 792 58

Using an adult mouse aortic-banded model of pressure-overload hypertrophy and isolated cardiomyocyte mechanics studies, we examined the hypothesis that contractile depression is due to altered cardiac contractile proteins rather than changes in left ventricular (LV) geometry, loading, or the extracellular matrix. FVB mice were banded at the transverse aortic arch or sham operated and studied after 7 days. In nine animals the gradient across the aortic band averaged 47 +/- 4 mmHg. Compared with sham-operated controls, banded animals had increased LV weight-to-body weight ratio (2.8 +/- 0.1 and 3.5 +/- 0.1, respectively; P = 0.035). Left ventricles from additional age-matched groups of mice that underwent identical surgical procedures were examined for altered transcriptional control of myosin heavy chains (MHCs). beta-MHC protein content increased (15 +/- 2%) vs. shams (3.8 +/- 2%; P = 0.004). Dot blots of LV RNA showed a corresponding increase in beta-MHC transcripts in banded animals (15.8 +/- 2%) vs. controls (5.7 +/- 2%; P = 0.012). Contractile performance was assessed using enzymatically disaggregated isolated LV myocytes paced at 0.5 Hz. There was no difference in percentage myocyte shortening between banded (8.6 +/- 0.5%) and control (9.1 +/- 0.5%) animals. However, maximal velocity of contraction was depressed after aortic banding (129 +/- 11 vs. 233 +/- 28 microns/s; P = 0.007), as was velocity of relaxation (105 +/- 11 vs. 188 +/- 22 microns/s; P = 0.007). These results suggest that depressed myocyte contractility after induction of pressure-overload hypertrophy in aortic-banded mice may be, in part, a consequence of transcriptional upregulation of the beta-MHC.
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PMID:Myosin heavy chain regulation and myocyte contractile depression after LV hypertrophy in aortic-banded mice. 804 5

Changes of ischemic myocardium following coronary occlusion, including active and passive functions, and adaptive changes of non-ischemic surviving myocardium have been summarized under the term "left ventricular remodeling" post myocardial infarction. An increase in left ventricular volume may be a consequence, and associated with an adverse prognosis. Although left ventricular dilatation may increase stroke volume and, thus, be compensatory at first, in about one-fifth of patients it ultimately results in progressive dysfunction and heart failure. Major determinants of this process are time, infarct size, infarct location, global left ventricular function assessed 4 days after infarction by radionuclide ejection fraction and right heart catheter (stroke volume), and morphology of the infarct-associated coronary artery. The surviving myocardium hypertrophies and may also dilate structurally. Depression of left ventricular ejection fraction chronically after the infarct is due to deterioration of wall motion of chamber segments initially classified normal by radionuclide analysis. Biochemical changes may also occur, including reduction of phosphocreatine, prolongation of time to peak Cai2+, and changes in myosin isoforms. Systemic or local humoral factors may be involved in these changes, however, clear evidence is still lacking. Perfusion of surviving myocardium may be altered under various conditions due to morphologic and functional changes of coronary vasculature. Successful prevention of heart failure and death by angiotensin converting enzyme inhibitors in asymptomatic patients with left ventricular dysfunction post-myocardial infarction has supported the pathophysiologic concepts of remodeling.
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PMID:Ventricular remodeling after myocardial infarction. Experimental and clinical studies. 835 28

1. Single fibres isolated from the anterior tibialis muscle of Rana temporaria were allowed to shorten against a high load during a 2.5-4.0 s fused tetanus (1-3 degrees C) and the maximum force produced at the short length was compared with that recorded during a fixed-end tetanus at the same overall fibre length. Changes in length of marked, consecutive segments (ca 0.5 mm in length) along the fibre were measured throughout the tetanus using a photoelectric recording system. 2. Loaded shortening (load ca 3/4 of maximum tetanic force) starting from approximately 2.55 microns sarcomere length and ending near slack fibre length depressed the tetanic force by 13 +/- 2% (mean +/- S.E.M., n = 10) and caused a marked redistribution of sarcomere length along the fibre. Unloaded shortening over the same range caused no force deficit and did not lead to increased dispersion of sarcomere length. 3. Loaded shortening below slack length produced less force depression and less non-uniformity of sarcomere length than did a corresponding intervention above slack length. 4. The force deficit after loaded shortening, both above and below slack fibre length, was positively correlated (P < 0.005) to the coefficient of variation of the sarcomere length along the fibre. 5. The decrease in active force after loaded shortening, and its relation to increased dispersion of sarcomere length along the fibre, could be simulated closely by a computer model in which the muscle fibre was assumed to consist of eleven discrete segments acting in series with a passive elastic element. 6. Experiments were performed in which the length of an individual segment of the intact muscle fibre was strictly controlled throughout a tetanus. Loaded shortening of such a 'length-clamped' segment caused no force depression during the subsequent isometric phase either above or below slack fibre length. 7. The results suggest strongly that force depression after loaded shortening of a single muscle fibre is attributable to non-uniform sarcomere behaviour along the fibre. The experimental evidence supports the view that: (i) the myosin cross-bridges act as independent force generators; and (ii) their steady-state performance during a tetanus is unaffected by the preceding contractile activity.
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PMID:Depression of tetanic force induced by loaded shortening of frog muscle fibres. 841 Jul 5

Myofibrillar but not actomyosin ATPase is depressed in failing myocardium from patients with dilated cardiomyopathy. Since there is a similar depression of myofibrillar ATPase in mitral regurgitation myocardium, we investigated whether or not the hydrolytic and mechanical performances of myosin are altered by comparing the maximal actomyosin ATPase activity and the in vitro myosin motility of myocardial myosin from patients with mitral regurgitation heart failure with that of patients with normal ventricular function. The results show that there is no significant difference (P > .05) between nonfailing and failing values for either the maximal actomyosin ATPase activity (0.3 s-1.head-1) or the myosin motility (1 micron/s). These observations suggest that changes, other than in the myosin heavy chain, contribute to the altered myocardial performance in mitral regurgitation myocardium.
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PMID:Maximal actomyosin ATPase activity and in vitro myosin motility are unaltered in human mitral regurgitation heart failure. 875 98

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