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)

Monoclonal antibodies against gizzard smooth muscle myosin were generated and characterized. One of these antibodies, designated MM-2, recognized the 17-kDa light chain and modulated the ATPase activities and hydrodynamic properties of smooth muscle myosin. Rotary shadowing electron microscopy showed that MM-2 binds 51 (+/- 25) A from the head-rod junction. The depression of Ca2+- and Mg2+-ATPase activities of myosin and Ca2+-ATPase activity of heavy meromyosin at low KCl concentration were abolished by MM-2. Viscosity measurement indicated that MM-2 inhibits the transition of 6 S myosin to 10 S myosin. While the rate of the production of subfragment-1 by papain proteolysis of 6 S myosin was inhibited by MM-2, the rate of proteolysis of the heavy chain of 10 S myosin was enhanced by MM-2 and reached the same rate as that of 6 S myosin plus MM-2. These results suggest that MM-2 inhibits the formation of 10 S myosin by binding to the 17-kDa light chain which is localized at the head-neck region of the myosin molecule. MM-2 increased the Vmax of actin-activated Mg2+-ATPase activities of both dephosphorylated myosin and dephosphorylated heavy meromyosin about 10- and 20-fold, respectively. MM-2 also activated the actin-activated Mg2+-ATPase activity of phosphorylated myosin at a low MgCl2 concentration and thus abolished the Mg2+-dependence of acto phosphorylated myosin ATPase activity. These results suggest that MM-2 inhibits the formation of 10 S myosin, and this results in the activation of actin-activated Mg2+-ATPase activity even in the absence of phosphorylation.
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PMID:Inhibition of conformational change in smooth muscle myosin by a monoclonal antibody against the 17-kDa light chain. 246 45

Three and 11 wk after coronary artery ligation in rats, the right and left ventricular free wall, septum, and papillary muscles from infarcted and sham-operated hearts were analyzed to determine whether regional variability existed in cardiac actomyosin adenosine triphosphate (ATPase) activity and myosin isoenzymes. Infarction produced a 74% greater right ventricular mass and 19% greater septal mass compared with sham-operated hearts at 3 wk. There was no additional increase in cardiac mass associated with infarction from 3 to 11 wk above that expected for normal growth. Actomyosin ATPase activity and the percent V1 myosin heavy-chain isoenzyme decreased significantly in all regions of the infarcted heart by 3 wk. In addition, the left ventricular and papillary muscle of infarcted hearts exhibited a decrease in percent V1 myosin of 18 and 35%, respectively, compared with the right ventricular free wall and septum. These differences persisted at 11 wk, although no further depression of actomyosin ATPase activity or shift in myosin isoenzyme distribution were observed over the 8-wk period. These results demonstrate that myocardial infarction induces a shift in the myosin isoenzyme distribution and depression in actomyosin ATPase activity of surviving cardiac tissue. Regional variability in myosin isoenzymes is evident by 3 wk, but additional adaptation in cardiac mass and myosin biochemistry do not occur beyond this time.
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PMID:Regional variation in rat cardiac myosin isoenzymes and ATPase activity after infarction. 252 83

The responses of muscle spindles in the iliofibularis muscle of the cane toad Bufo marinus were examined during constant velocity stretch of the passive muscle. Spindles were found to show an 'initial burst' of high frequency impulses at the onset of stretch. Associated with the initial burst was a steep passive tension rise in the whole muscle, the short-range elastic component (Hill, 1968), called here the passive stiffness. The size of the initial burst was found to depend on muscle length in a similar way as whole-muscle tetanic tension. Repetitive stretch was found to reduce both the initial burst and passive stiffness. The time taken for both to return to their control values was 3 and 10 s respectively. If immediately following repetitive stretch the muscle, and hence the spindle, was held stretched for 3 s, the initial burst in response to a subsequent stretch from a shorter length remained reduced in size for 300 s. The depression could be reversed by a brief period of fusimotor stimulation. Hypertonic Ringer solutions were found to increase the initial burst and passive stiffness, while both were reduced in hypotonic solutions. Low concentrations of caffeine (1.5 mM) produced a similar decrease in both the initial burst and the passive stiffness. Calcium-free Ringer solution left the stiffness unchanged, and increased the whole dynamic response of the spindle. Metabolic exhaustion and poisoning of the muscle caused the initial burst to increase while decreasing the active tension. It is concluded that the initial burst is an intrafusal manifestation of the passive short-range stiffness of extrafusal muscle which is thought to be due to the formation of stable cross-bridges between the actin and myosin filaments of myofibrils.
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PMID:The initial burst of impulses in responses of toad muscle spindles during stretch. 293 46

Previous studies in hearts of female rats have demonstrated that ventricular hypertrophy due to systolic overload, when combined with hypertrophy induced by a chronic swimming program, results in increased cardiac performance and enhanced contractile protein activity compared with the effects of hypertension alone. To explore how a chronic running program affects the function of hypertensive hearts, renal hypertension was created in female rats, and the animals were subjected to a program of chronic treadmill running. Running alone caused enhanced cardiac function, an increase in myosin adenosinetriphosphatase (ATPase) activity, and an increase in the percent of the V1 myosin isoenzyme. Hypertension alone caused cardiac hypertrophy with a depression in myosin ATPase activity and a decrease in the percent of the V1 isoenzyme. Running improved cardiac function in hearts of normotensive rats but had no effect in hearts of hypertensive rats. Despite the diminished myosin ATPase activity in hearts of hypertensive runners and the decrease in percent of the V1 isoenzyme, cardiac function was well maintained. The results demonstrate that a chronic running program in hypertensive rats, in contrast to a chronic swimming program, had virtually no effect on cardiac performance or contractile proteins. The dissociation between myocardial performance and the contractile proteins implicates other biochemical mechanisms in the adaptations observed.
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PMID:Combined effects of hypertension and chronic running program on rat heart. 295 51

1. Since it has been demonstrated that trifluoperazine (TFP) increases the affinity for Ca2+ of troponin C as well as calmodulin, the effect of TFP was examined on the Ca2+-induced tension in mechanically skinned fibres isolated from frog skeletal muscle and on Ca2+-dependent ATPase activity of myofibrils from similar frog skeletal muscle. 2. Lower concentrations of TFP increased the Ca2+ sensitivity of myofibrils without a change in the maximum tension, giving rise to a less steep tension-pCa relationship. This effect was reversible although thorough washes were necessary. The drug also enhanced myofibrillar ATPase activity, not only at low Ca2+ concentrations but also at saturating high Ca2+ concentrations. The increased affinity of troponin C for Ca2+ is difficult to accept as the sole explanation for the stimulatory effect of TFP. 3. Half of the maximum stimulating effect was obtained between 10 and 30 microM-TFP, which is similar to the reported apparent inhibition constant (Ki) for calmodulin-dependent enzyme reactions. However, the stimulating effect of TFP cannot be attributed to its inhibition of calmodulin because of the finding that this effect was independent of Ca2+. Earlier published results (e.g. Klee & Vanaman, 1982) also support this conclusion. 4. Studies on myofibrillar ATPase activity suggest that the stimulating effect of TFP is not identical in its underlying action with those of caffeine and quercetin, which are also known as Ca2+-sensitizing drugs, having a similar eventual effect on tension development. 5. Higher concentrations of TFP decreased the maximum tension induced by high concentrations of Ca2+, while enhancing the tension in the presence of low concentrations of Ca2+. Analogous findings for ATPase activity were also made. TFP concentration for half the maximum depression was about 10 times higher than that for half the maximum stimulation. This suggests that different site(s) are involved in the stimulatory and inhibitory effects of TFP, although there may be some sites in common. 6. Discussion favours the stimulating effects of TFP as being caused considerably by the affected molecular interactions among myosin, actin, tropomyosin and troponin.
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PMID:Increase by trifluoperazine in calcium sensitivity of myofibrils in a skinned fibre from frog skeletal muscle. 297 64

1. Adult soleus muscles were denervated and stimulated directly for 2-130 days with 'fast' (short pulse trains at 100 Hz) or 'slow' (continuously at 10 Hz, or long pulse trains at 15 Hz) stimulus patterns. 2. At the end of the period of stimulation isometric twitches and tetani and isotonic shortening velocities were measured. Frozen cross-sections were later examined with antibodies against myosin heavy chains specific for adult fast, adult slow and fetal myosin. 3. Isometric twitch duration (twitch time-to-peak and half-relaxation time) decreased during intermittent 100 Hz stimulation to values that were almost as fast as in the normal extensor digitorum longus (EDL) (95 and 94% transformation). The major part of the decrease occurred between 2 and 21 days after the onset of stimulation, and was accompanied by post-tetanic potentiation of the twitch, 'sag' in tension during an unfused tetanus, lower twitch/tetanus ratio and marked shifts to the right (higher frequencies) of the tension-frequency curve of the muscle. In contrast, during 10 or 15 Hz stimulation the isometric twitch duration remained slow, the twitch continued to show post-tetanic depression and absence of 'sag', while the twitch/tetanus ratio increased. 4. Denervation per se led to a slight increase and, then, after about a month, to a moderate and gradual decrease in twitch duration. The twitch/tetanus ratio increased markedly and post-tetanic depression became less pronounced or disappeared. Muscle weight and particularly tetanic tension were markedly reduced and these reductions were to a large extent counteracted by electrical stimulation. 5. Implantation of sham electrodes had no effect on twitch duration of denervated or innervated control muscles, but reduced tetanic tension in the innervated control muscles. 6. Maximum isotonic shortening velocity of the whole muscle (mm/s) increased during intermittent 100 Hz stimulation to a value as fast as in the normal EDL (110% transformation). Since the muscle fibres also increased in length (35%) maximum intrinsic shortening velocity (fibre lengths/s) was only incompletely transformed (55%). The increase in Vmax occurred between 7 and 14 days after the onset of stimulation. 7. All the fibres stimulated intermittently at 100 Hz were strongly labelled with anti-fast myosin and more than 90% were in addition weakly labelled by anti-slow myosin. Weak and variable labelling with anti-fast myosin was first detected 7 days after the onset of stimulation. In contrast, essentially all the fibres stimulated at 10 or 15 Hz showed no binding of anti-fast but strong binding of anti-slow myosin.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Slow-to-fast transformation of denervated soleus muscles by chronic high-frequency stimulation in the rat. 323 51

Prolonged ingestion of ethanol may lead to a cardiomyopathy, and studies in the experimental animal have demonstrated alterations in protein metabolism. These changes include depression of protein synthesis with acetaldehyde in the acute experiment, in vitro, and after chronic ethanol ingestion in vivo. The present studies were initiated to see if the inhibition of protein synthesis following prolonged ethanol ingestion involved myocardial contractile proteins. Newly weaned guinea pigs, weighing 350 g, were placed on a regimen of normal laboratory diet with 10% ethanol in the drinking water. Calorie-matched controls, drinking dextromaltose in the water, were simultaneously run. After 40 weeks of ingesting 10% ethanol in the drinking water, hearts from growing guinea pigs were removed and synthesis of myocardial contractile proteins (myosin heavy chains, light chains (LC1, LC2), actin, and tropomyosin) assayed in vitro with 3H-labeled amino acids. With aging, there was a decrease in the rates of synthesis of all the contractile proteins. After 40 weeks of ethanol ingestion, the synthetic rates of myosin heavy and light chains and tropomyosin were the same as in calorie-matched controls, but the synthetic rate of actin was significantly decreased by 20% (p less than 0.01). This decrease in actin synthesis may be the first indication of ultimate inhibition of synthesis of all the contractile proteins which may lead to myofibrillar disorganization and vacuolization reported after chronic ethanol ingestion.
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PMID:Prolonged feeding of ethanol to the young growing guinea pig. III. Effect on the synthesis of the myocardial contractile proteins. 354 78

Intestinal smooth myosin B was prepared from muscle layers around the lesion in dogs with experimental colonic stenosis and in patients with congenital intestinal obstruction. Mg2+-ATPase activity of the myosin B was compared between the proximal dilated segment and distal segment to obstruction. Experimental colonic stenosis: In early period after surgery, proximal colons showed higher activity of myosin B ATPase than distal colons, decreasing to less than distal colon as time passed. Congenital intestinal obstruction: In three cases, whose atresia might have occurred at earlier period of gestation, proximal bowels showed less activity of myosin B ATPase than distal bowels. However, in two cases, whose atresia might have occurred at later period of gestation, and two cases with intestinal stenosis, proximal bowels indicated higher activity of myosin B ATPase than distal bowels. These data suggested that the contractibility of the proximal intestine was depending on the duration of obstruction, and it was depressed in the former patients and was accelerated in the latter patients. These results suggested that the extensive resection of dilated proximal bowel in the congenital atresia is not always necessary to obtain good postoperative intestinal dynamics at the operation of the atresial lesions which may be induced at later period of gestation. They also suggested that surgery for intestinal obstruction should be performed before the depression of intestinal contractibility to get good bowel function.
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PMID:[Myosin B ATPase activity of the intestinal smooth muscle in intestinal obstruction]. 614 39

Cardiac hypertrophy, induced by pressure overload, leads to a depression in the rate of force development, velocity of shortening, tension-dependent heat generation, and myosin ATPase activity, whereas cardiac hypertrophy, induced by thyroxine administration, leads to an increase in these parameters. These changes have been attributed, in part, to structural changes in myosin. In this study, we have investigated changes in the relative content of myosin isozymes and differences in primary structure of the isozymes in pressure-overloaded and thyrotoxic cardiac hypertrophy in the rabbit. Three myosin isozymic forms (V1 = fastest, V2 = intermediate, V3 = slowest mobility) were observed in pyrophosphate polyacrylamide gels from normal hearts with the V3 component being the predominant species. In the pressure-overloaded model, the V1 and V2 components disappeared or were present in reduced amounts leaving the V3 more predominant. The most striking difference was the isozymic profile produced in thyrotoxic hearts where the V1 became the predominant component and V2 and V3 the minor components. alpha-Chymotryptic digestion of myosin heavy chains produced characteristic, reproducible peptide patterns for each of the animal models, as did fluorographic analyses of alpha-chymotryptic digests of 14C-iodoacetamide (IAA)-labeled SH1 peptides of myosin. Our results suggest that altered proportions of myosin isozymes may be responsible for altered cardiac performance.
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PMID:Altered myosin isozyme patterns from pressure-overloaded and thyrotoxic hypertrophied rabbit hearts. 621 Dec 93

The effect of divalent cations on the self-association of high molecular weight subfragment-2 (long S-2) and low molecular weight subfragment-2 (short S-2) of rabbit skeletal muscle myosin has been investigated. In the presence of millimolar concentrations of Ca2+ or Mg2+ long S-2 associates at neutral pH to form ordered, high molecular weight aggregates whereas short S-2 does not associate. The association process is co-operative and results from binding two to four divalent cations within the light meromyosin-heavy meromyosin (LMM-HMM) hinge region of long S-2. Optical diffraction of electron micrographs of the long S-2 aggregates revealed several periodicities including reflections near 143 A. High molecular weight HMM showed a similar divalent metal induced self-association. Chymotryptic digestion studies of rod filaments reveal that cleavage within the LMM-HMM hinge is also strongly dependent on the presence of divalent cations. At pH 8, in the absence of divalent cations, the S-2 region appears to be displaced away from the filament backbone resulting in rapid proteolysis in the hinge domain. At high cation concentrations (greater than 10 mM) proteolytic cleavage is suppressed. A similar depression of the (substantially lower) hinge cleavage rate was also observed at neutral pH following addition of these divalent metal ions. Results suggest that binding of Mg2+ within the hinge domain under physiological conditions may act to lock the cross-bridge onto the thick filament surface in its resting-state orientation.
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PMID:Self-association of a high molecular weight subfragment-2 of myosin induced by divalent metal ions. 635 Jun

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