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At least 19 recordsLinked to original sources
PubMed1978

Correlation between the effects of salbutamol on contractions and cyclic AMP content of isolated fast-and slow-contracting muscles of the guinea pig.

The effects of isoprenaline and salbutamol on incomplete tetanic contractions of the isolated soleus (slow contracting) and extensor digitorum longus (EDL-fast-contracting) muscles of the guinea pig were studied and an attempt made to correlate these effects on contractility with changes in cyclic AMP concentrations. Salbutamol was 10-12 times less potent than (+/-)isoprenaline in decreasing the force of subtetanic contractions in the soleus and between 5-6 times less potent in increasing the force of subtetanic contractions in the EDL. This observation plus the lack of activity of both the selective beta1-adrenoceptor antagonist (atenolol) and the selective beta1 agonist (H 133/22) in the EDL implies involvement of beta2-adrenoceptors in these responses of the muscles to isoprenaline and salbutamol. The soleus muscle was about 6-12 times more sensitive to effects of beta-adrenoceptor agonists than the EDL. In concentrations which produced effects on muscle contractility, salbutamol significantly elevated cyclic AMP concentrations in both types of muscle. These effects were antagonised by propranolol. It seems clear that the contrasting effects of sympathomimetic amines on slow-and fast contracting muscle are mediated through a common mechanism-elevation of cyclic AMP. Possible explanations of this apparent paradox are discussed.

Albuterol↗
PubMedDate not supplied

[Relationship between the amplitude of myocardial contractions in frogs and the frequency of electrical stimulation. Role of external and intracellular calcium in the coupling of excitation and contraction].

Ionic currents were studied on the frog atrial trabeculae (Rana ridibunda) at 20 degrees C using a double sucrose gap voltage clamp arrangement. The net inward current peaks did not change in the course of repetitive stimulation (0,5/s) in contrast to the increase of the contraction amplitude (isometric tension) in the similar conditions (Bowdich staircase). The slow component of the net inward current revealed under the action of TTX (2-10(-8) g/ml) was increased upon the increase of external Ca concentration but was blocked when D-600 was introduced into the solution. The inhibitory action of D-600 on the contraction amplitude was frequency independent (in the ranges: 0,1--0,7/s). The decrease of external Na+ (isoosmotic replacement of 70% NaCl by sucrose) or the increase (5-fold) of the external Ca2+ significantly enhanced the myocardial contraction depressed with D-600. However these contractions fall in the course of rhythmical stimulation, and the effect being strongly dependent on the rate of stimulation. The results confirm the assumption (see: Biophysics, 6, 1024, 1976), that intracellular Ca stores (sarcoplasmic reticulum, internal surface of the cellular membrane) are involved in the control of the contractility in the amphibian myocardial cells. Many peculiarities of the excitation-contraction coupling in the frog myocardial cells can be explaned if one assumes that: 1) there is no space separation of primary uptake and release of Ca ion sites in the frog myocardium; 2) the system of "resting Ca chanels" in the frog myocardial cells is not so well developed as in the mammalian myocardial cells.

Animals↗
PubMed1975

Myosin aggregates as a requirement for contraction and a proposal to the mechanism of contraction of actomyosin systems.

Glycerinated fibers of rabbit psoas muscle showed no augmentation of tension development upon incubation with heavy meromyosin, irrespective of whether the fibers were of standard length, stretched, or extracted of their myosin content. The effect of heavy meromyosin was to suppress contraction. These observations are in disagreement with certain recent published reports (Oplatka et al., 1974) and do tend to support the current sliding filament theory of muscle contraction and the necessity of bipolar myosin filaments for contraction. A possible mechanism of contraction in protein systems, including tension generation in actomyosin fibers and superprecipitation, is described emphasizing the polarity of both myosin and actin filaments.

Actins↗
PubMed1975

Acid-base changes and excitation-contraction coupling in rabbit myocardium. I. Effects on isometric tension development at different contraction frequencies.

The effects of changes in acid-base parameters on the active force of isolated rabbit papillary muscles were studied at contraction frequencies of 12, 60 and 120/min. When extracellular pH was lowered from 7.4 to 7.0 and 6.7 in a bathing solution buffered with 10 mM histidine, the active force decreased at all contraction frequencies studied. After parallel increases of HCO3-minus concentration (up to 47 mM) and PCO2 at a constant extracellular pH of 7.4 the active force of the muscle increased at low and decreased at high contraction frequencies. None of these effects can be attributed to catecholamine release or to altered extracellular concentration of ionized calcium. The inotropic effects produced by bicarbonate were not reproducible by methyl sulfate (47 mM) or propionate (47 mM). It is concluded that: 1. a lowering of the extracellular pH has a negative inotropic effect at all frequencies, 2. HCO3-minus has a positive inotropic effect that is most pronounced at low contraction frequencies and 3. CO2 has a negative inotropic effect exceeding that produced by the mere reduction in extracellular pH. The cellular mechanisms involved in the various inotropic effects are discussed.

Animals↗
PubMed1978

[Effect of neural regulation on the fluctuations in the intervals between cardiac contractions and the force of the contractions].

Statistical analysis of the cardiac rhythm according to the R--R intervals and the force of contractions according to their amplitude was undertaken. The variation coefficient (N%) reflecting the degree of irregularity of intervals between the contractions and the force of contractions during maximum cardiac hyperfunction induced by clamping the aorta for 30 sec was determined. Vagotomy led to a decrease in the irregularity for cardiac rhythm and force of cardiac contractions.

Animals↗
PubMed1979

Role of calcium and cyclic adenosine 3':5' monophosphate in regulating smooth muscle contraction. Mechanisms of excitation-contraction coupling in smooth muscle.

Caclium initiates smooth muscle contraction by activating an enzyme, myosin light chain kinase. This enzyme catalyzes the transfer of phosphate from adenosine triphosphate to the 20,000 dalton light chain of myosin. In its phosphorylated form myosin interacts with actin to produce muscle contraction. The mechanism by which calcium activates myosin kinase requires (1) the binding of calcium to a 16,500 dalton calcium-binding protein (calmodulin), and (2) the binding of calmodulin-calcium to a 125,000 dalton catalytic subunit. This two protein complex is the active form of myosin light chain kinase. Smooth muscle relaxation is mediated by cyclic adenosine 3':5' monophosphate (cyclic AMP). One nechanism by which the latter may exert a direct effect on actin-myosin interaction is through the activation of a cyclic AMP-dependent protein kinase that can phosphorylate the 125,000 dalton component of myosin light chain kinase. Phosphorylation of myosin light chain kinase decreases the activity of the enzyme, thus favoring the unphosphorylated form of myosin, which cannot interact with actin to produce smooth muscle contraction.

Actins↗
PubMed1977

Oscillating contractions in protoplasmic strands of Physarum: effects of external Ca++-depletion and Ca++-antagonistic drugs on intrinsic contraction automaticity.

1. The minimal requirement of external Ca-concentration for continuance of contraction activity lies in the range of 10(-4) M. 2. As in mammalian smooth muscle, the Ca antagonistic drugs verapamil and D 600 (5.10(-4) M) suppress the minute-rhythms. The action of the drugs is inhibited by 5mM Ca, La or Mn. De novo generation of contraction automaticity is not inhibited by external Ca depletion or by Ca antagonists. 3. It is concluded that rhythmical Ca fluxes across the cortical plasmalemma are not a precondition for triggering continuance or de novo generation of contraction automaticity.

Calcium↗
PubMed1978

Effect of inhibitors of slow calcium current on rested state contraction of papillary muscles and post rest contractions of atrial muscle of the cat and rabbit hearts.

Effect of Ni, Co and Mn ions and of D-600 on rested state contractions (RSCs) of cat and rabbit papillary muscles and on post rest contractions (PRCs) of cat and rabbit atrial muscle was investigated. Ni and Co in concentration 2 mmol/l reduced the force of RSCs in papillary muscles by 78%, increased the dip between the phase 1 and 2 of respective action potentials (APs), lowered the level of plateau and decreased the total duration of AP. Strong PRCs in atrial muscle were reduced by Ni only by 25%, while the subsequent beats were strongly inhibited. Ni completely inhibited RSCs in papillary muscles increased by caffeine (10 mmol/1) or by reduction in Na concentration by 50%. Mn ions in concentration 1--2 mmol/l inhibited strongly both RSCs in papillary muscles and strong PRCs in atrial muscle, increased the dip between phase 1 and 2 and increased total duration of AP. Mn ions stimulated 45Ca efflux from papillary muscles and atrial strips. D-600 did not affect RSCs nor the shape of respective APs. It is concluded that RSCs in papillary muscles are directly activated by Ca inflow during the respective excitation while strong PRCs in atrial muscle are activated mostly by Ca released from intracellular stores.

Action Potentials↗
PubMed1975

Ultrastructure of the contractile system of striated skeletal muscle and the processes of muscular contraction. II. Releasing system and mechanisms of muscular contraction.

The tropomyosin-troponin system of the thin filaments acts as a regulator of the interaction of myosin with actin by a process of inhibition. This inhibition is released by Ca2+ ions. Muscle contraction occurs when Ca+2 ions are released from the sarcoplasmic reticulum into the myofibril, where they interact with the troponin of the thin filaments. Muscular contraction is due to the sliding of the two kinds of filaments past each other in the hexagonal network of the myofibril. Many hypotheses have been formulated concerning the intimate molecular mechanisms responsible for the sliding of the filaments past each other, but none of these can be considered to be entirely satisfactory.

Actins↗
PubMed1979

A histological comparison of contracted and non-contracted capsules around silicone breast implants.

A single blind comparison of capsular tissue obtained from both breasts from 7 patients in whom unilateral contracture had occurred leads to the following conclusions: (1) The presence of droplets (presumed to be silicone, or extractable silicone as identified by IR) in capsular tissue does not correlate with the clinical finding of firmness. (2) Contracted capsules are apt to be significantly more cellular, largely as a result of an increased fibroblast population. (3) The apparent severity of inflammation in a biopsy of a capsule does not correlate with the clinical degree of firmness in the breast. (4) In the 7 cases studied, capsule thickness or vascularity, collagen alignment, staining uptake, presence of foreign bodies, or presence of an inner cell layer of macrophages did not correlate with the clinical finding of firmness.

Breast↗
PubMed1979

Excitation-contraction coupling in normal and myopathic hamster hearts I: identification of a calcium pool involved in contraction.

The results of this study indicate that two min of Ca-free perfusion did not significantly alter the exchange kinetics of mannitol or Ca in isolated heart preparations. A numerical solution for series Ca exchange between a superficial Ca pool, Ca1, and an intracellular pool, Ca2, was developed in terms of the coefficients and constants determined from a parallel analysis. The series and parallel models for Ca efflux yielded a high correlation between contractile activity and the rate of exchange and Ca content of Ca1. The kinetics of Ca influx were best described by a series model of exchange and agreed closely with the Ca contents and exchange properties measured during Ca efflux. No differences were detected between normal and myopathic hamster hearts in the kinetics of Ca exchange or the role of Ca1 in the E-C coupling process.

Animals↗