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Biomedical subjects

G Suarez-Kurtz

Publications and source records attributed to G Suarez-Kurtz.

At least 73 records · Page 4Linked to original sources
PubMed1983

Enzyme release from skeletal muscle.

Several factors that modify the release of sarcoplasmic enzymes from skeletal muscle, with emphasis on data from isolated frog muscles, are reviewed. The evidence indicates that creatine kinase (CK) and lactate dehydrogenase (LDH) are released continuously from frog muscle fibers that have normal resting potentials and are presumably bound by an intact plasma membrane. The rates of release are determined not only by the transsarcolemmal efflux rates but also by the kinetics of the enzyme diffusion in the extracellular space. The release of CK and LDH is increased by sarcolemmal injury but is also stimulated by procedures that do not cause irreversible damage to membrane integrity as judged from morphological and electrophysiological parameters. Among these procedures are step changes in the tonicity of the bathing medium and brief exposure to nanomolar concentrations of polylysine or polyornithine, which increase the release rates from frog muscles by one order of magnitude. The possible mechanisms responsible for the efflux of sarcoplasmic enzymes and the relevance of these data to the increased enzyme loss from the muscles of patients with neuromuscular diseases are discussed.

Animals↗
PubMed1982

The role of calcium in excitation--contraction coupling in crustacean muscle fibers.

The evidence that calcium (Ca) plays an important role in electrical activity and an essential role in excitation--contraction (E--C) coupling in crustacean muscles is reviewed. These muscles produce graded electrical and mechanical responses to applied depolarizations. Removal of Ca from the bath solution eliminates both responses. Addition of Ba2+ or Sr2+ to Ca-free saline restores membrane electrogenesis, and all-or-none action potentials can be induced. With Sr2+ vigorous contractions are produced, whereas Ba action potentials evoke minimal or no tension, showing that rapid depolarization of the membrane potential is not sufficient per se for E--C coupling in crab and barnacle muscle. Several inorganic (e.g., multivalent cations) and organic (e.g., aminoglycoside antibiotics) which block membrane Ca channels block electrogenesis and contraction. However, the "Ca antagonists" verapamil and D600 also block Ca uptake at intracellular storage sites, resulting in spontaneous contractions and the delayed relaxation of small contractions associated with residual Ca currents. The evidence that the Ca which enters the fibres needs to release Ca from intracellular storage sites to produce contractions is detailed and discussed. Finally, a model for E--C coupling is discussed. This model includes the sites and mechanisms of action for several chemicals which modify E--C coupling in crustacean muscle fibres.

Action Potentials↗
PubMed1982

Release of creatine kinase from frog muscle by osmotic changes.

The rate of creatine kinase (CK) release from isolated frog extensor longus digiti IV ("toe") muscle increased on transfer from the control Ringer solution (referred to as 1.0 T) to a hyperosmotic solution (1.0 T plus 400 mM glycerol) or to hypertonic solutions (1.5-2.5 T) prepared by addition of NaCl or sucrose to 1.0 T. On return to 1.0 T, CK release rate was further elevated, reaching peak values (14.4- and 12-fold above the basal value, respectively, with the glycerol treatment and with solution 2.5 T) within 10-15 min and declining subsequently toward base line. Although the stimulation of CK release by changes in external tonicity increased with the magnitude of the osmotic step change, there was no enhancement of release when the tonicity changes were performed gradually in 0.1-T steps at 1-min intervals. The stimulation of CK release by tonicity changes cannot be ascribed to irreversible loss of functional integrity of the surface or tubular membranes or to CK diffusion through aqueous pores. The possibility that an exocytosislike process is involved is discussed.

Animals↗
PubMed1982

Release of creatine kinase and lactate dehydrogenase from frog skeletal muscles treated with imipramine.

Frog sartorius and extensor longus digiti IV ("toe") muscles were mounted in sample collecting units, isometric tension was recorded and the activities of creatine kinase and lactate dehydrogenase released into the bathing medium were measured. Addition of imipramine (greater than 0.2 mM) to the control medium induced muscle contractures and increased the rates of enzyme release. Electronmicrographs of muscles exposed to imipramine (0.5--1.0 mM) showed fibers in which the extracellular marked horseradish peroxidase was detected in the sarcoplasm. Both the enzyme-releasing and the contractile effects of imipramine were inhibited by procaine (but not by lidocaine) and were enhanced by replacement of external chloride ions with propionate. The data are consistent with the suggestion that events associated with tension development contribute greatly to the imipramine-induced loss of sarcoplasmic enzymes from frog skeletal muscles. The elevated Ca++ concentration in the sarcoplasm during the imipramine-induced contracture is thought to lead to changes in the plasma membrane that account for the increased enzyme loss and for the penetration of horseradish peroxidase into the sarcoplasm.

Animals↗
PubMed1982

Caffeine and quinine increase the release of sarcoplasmic enzymes from frog skeletal muscles.

1. The rates of release of two sarcoplasmic enzymes, creatine kinase and lactate dehydrogenase, from frog skeletal muscle were increased by caffeine and by quinine at concentrations that induced muscle contractures. 2. Pre-treatment with procaine blocked both the contractures and the increased enzyme loss induced by these alkaloids. 3. It is suggested that the prolonged increases of the Ca2+ concentration in the myofibrillar space during the drug-induced contractures lead to membrane injury and to an increase in the loss of sarcoplasmic enzymes from the muscle.

Animals↗
PubMed1982

Effects of hypertonicity on frog muscle contractures induced by quinine.

1. Frog sartorius and extensor longus digiti ("toe") muscles were used to investigate the effects of solutions of two (2T) and three (3T) times normal tonicity on the contractures elicited by quinine or by high-[K]O media, and on twitch and tetanic tension. 2. Solution 2T had no effect on the peak amplitude of quinine-induced contractures (PQ) of toe muscle but increased the PQ of sartorius muscle. Toe muscle PQ was significantly reduced by 3T. The quinine-induced contractures of sartorii bathed in 3T were slower than, but reached peak values not significantly different from, those obtained with control Ringer solution (1T). 3. The twitch and tetanic contractions of both sartorius and toe muscles were partially or totally blocked by 2T and were always abolished by solution 3T. 4. The maximal amplitude of K+-induced contractures (PK) of toe muscle was significantly reduced, but not abolished, by solutions 2T and 3T. The PK of sartorius muscle was greater at 2T than at 1T, but, in contrast to the transient tension recorded for 1T, the K+-induced contracture in solution 2T had a prolonged plateau. 5. The results suggest that hypertonicity affects the contractile apparatus as well as the excitation-contraction coupling process. The enhancement of quinine- and K+-induced contractures is ascribed to inhibitory effects of hypertonicity on Ca2+-sequestration by the sarcoplasmic reticulum.

Action Potentials↗
PubMed1981

Release of sarcoplasmic enzymes from frog skeletal muscle.

Isolated, intact frog muscles bathed in control saline release creatine kinase (CK) and lactate dehydrogenase (LDH) at constant rates for several hours. The basal rates of release from "toe" muscles (CK 0.087%/min; LDH 0.105%/min) were one order of magnitude greater than those from semitendinosus muscles. This is attributed to differences in muscle mass and geometry, and to the smaller diameter of toe muscle fibers. Enzyme release rates were not affected by Na-free or Cl-free solutions, whereas LDH release rate doubled during exposure to Ca-free (EGTA-containing) saline or in the presence of isosmotic solutions containing 120 mM KCl or potassium propionate. Following mechanical injury or detergent treatment (Brij 58), the enzyme release rates into Ca-free medium reached peak values 4 and 16 times (toe muscle), and 16 and 20-30 times (semitendinosus), respectively, the control rates. The greater effect of detergent treatment is ascribed to a larger area of sarcolemmal damage plus possible changes in the state of the enzymes in the sarcoplasm.

Animals↗
PubMed1979

Dissociation of action potentials from contraction in single crab muscle fibers.

In single crab fibers (Callinectes danae) bathed in Ca2+-free media, Ba2+ action potentials did not elicit tension. In contrast, Sr2+ spikes evoked twitches similar in amplitude to those accompanying the control Ca2+ spikes. Tension development in these fibers, therefore, depends on the ionic species carrying the inward current during membrane excitation. The Ca2" or Sr2+ influx appears insufficient to evoke the observed twitch tensions, and it seems necessary to postulate mobilization of an intracellular source of Ca1+. Procaine, which suppresses release of Ca2+ from sarcoplasmic reticulum, depressed twitch tension but did not reduce the overshoot or duration of Ca2+ or Sr2+ spikes. This finding is compatible with the suggestion that the contractions results from release of Ca2+ from the sarcoplasmic reticulum initiated by signals given by the influx of Ca2+ or Sr2+, but not Ba2+.

Action Potentials↗
PubMed1979

The depolarizing afterpotential of crab muscle fibres. A sodium-dependent process mediated by intracellular calcium.

1. A study was made of the depolarizing afterpotential (d.a.p.) which follows the initial graded electrogenesis of crab muscle fibres. 2. Increasing the strength, duration or amplitude of the stimulating current pulses enhanced both the d.a.p. and the local contractions. 3. Arsenazo III was injected intracellularly and changes in light absorbance by the dye were used to monitor the increase in free sarcoplasmic Ca concentration during excitation-contraction (E-C) coupling. The onset of the absorbance changes occurred during the depolarizing phase of the initial electrogenesis and the maximum value coincided with the peak of the d.a.p. An exponential decay of the absorbance signal occurred during the repolarizing phase of the d.a.p. 4. Ionophoretic injection of EGTA into the sarcoplasm did not affect the initial electrogenesis but did reduce changes in dye absorbance, blocked tension development and abolished the d.a.p. 5. Caffeine (0.1--0.4 mM) markedly enhanced both the d.a.p. and the local contractions, but had no effect on the initial electrogenesis. 6. Replacement of extracellular Na ions with Li, Tris or choline abolished the d.a.p. The initial electrogenesis was enhanced in the choline-containing medium, but was not affected by Li or Tris. The rate of relaxation of the local contractions and the rate of decay of the light absorbance changes were slowed in Na-free saline. 7. Tetrodotoxin (10(-5) g/ml.) had no effect on either the membrane responses or tension development. 8. For initial graded responses of comparable peak amplitude a threefold reduction of [Ca-a1o shortened the d.a.p., but had little effect onits peak amplitude. A fivefold increase in [Ca]o reduced both the amplitude and duration of the d.a.p. 9. Changes in [Mg]o had little effect on the d.a.p., but both Mn (4--10 mM) and La (0.1 mM) blocked the initial electrogenesis and the d.a.p. 10. It is concluded that distinct ionic mechanisms give rise to the initial electrogenesis and the d.a.p. While the former is due to activation of Ca conductance, the d.a.p. is a Na-dependent phenomenon that is tetrodotoxin-insensitive, and mediated by the rise of intracellular Ca concentration during E--C coupling.

Animals↗
PubMed1979

Inactivation of creatine kinase in physiological saline solutions.

To determine the optimal conditions for measuring the activity of creatine kinase released from isolated skeletal muscle preparations, we investigated the stability of the enzyme during storage in saline solutions of varying composition. Parameters studied were temperature, presence of albumin or dithiothreitol, calcium concentration and anionic composition. It is concluded that maximal activity is retained when samples are kept at 4 degrees C and analyzed within 24 hours in the presence of a thiol-protective compound. If longer storage periods are anticipated, inactivation is significantly retarded by addition of albumin or by decreasing the free calcium concentration of the storage salines.

Animals↗
PubMed1978

Competitive antagonism between calcium and aminoglycoside antibiotics on guinea-pig intestinal smooth muscle.

Streptomycin and related aminoglycoside antibiotics and magnesium ions antagonize in a competitive manner the contractile response elicited by calcium ion on the potassium-depolarized guinea-pig ileum. The inhibitory potency decreases in the following way: gentamicin greater than magnesium greater than neomycin greater than streptomycin=streptidine greater than kanamycin. Streptomycin was also found to reduce the uptake and to increase the efflux of 45Ca. To explain these effects two alternative mechanisms are proposed: 1) a competition of the antibiotics with calcium ions for binding sites of a transport system which carries the activator ion to the myoplasm, and 2) an interaction of the antibiotics with membrane sites that regulate calcium permeability with a consequent reduction of calcium passage to the cell.

Aminoglycosides↗
PubMed1977

Effects of verapamil on excitation-contraction coupling in single crab muscle fibers.

The effects of verapamil and its optical isomers on the electrical and mechanical characteristics of single muscle fibers of Callinectes danae were studied. Verapamil (10-20 microng/ml) blocked the procaine- and TEA-induced spikes; the blockade was preceded by reduction in the rate of rise of the upstroke and increase in the duration of the action potentials. Inhibition of Ba-spikes required higher concentrations of verapamil (greater than 50 microng/ml). These concentrations reduced the amplitude of the normally occurring graded electrogenic membrane responses and reduced the rate of development of the current-induced tensions. With lower concentrations (10-30 microng/ml) verapamil enhanced the negative afterpotentials and the peak amplitude of the local contractions elicited by depolarizing current pulses, while the graded membrane responses were not markedly modified. Verapamil (1-100 microng/ml) did not affect the resting membrane potential but increased the effective membrane resistance. Determination of the cable characteristics by DC pulses indicated that verapamil (1-10 microng/ml) shortens the membrane length constant, increases the specific resistivity of the sarcoplasm and, in most cases, increases the membrane time constant. Verapamil (10 microng/ml) induced tension in these crab fibers. The contractions were potentiated in Na-deficient media, by increase in [Ca]0, and by membrane depolarization; "Ca-free" salines depressed, and procaine abolished these contractions. The results suggest that verapamil affects both Ca and K conductances and interferes with the Ca-sequestering mechanisms of these fibers. The (-)-isomer of verapamil was more effective than the (+)-isomer with respect to tension development, prolongation and subsequent blockade of procaine-spikes and enhancement of current-induced after-potentials and contractions.

Animals↗
PubMed1977

Inhibition by hypertonic solutions of Ca-dependent electrogenesis in single crab muscle fibers.

This study describes the effect of hypertonic solutions on isolated muscle fibers of Callinectes danae. Solutions of twice normal tonicity (2.0 T) inhibit both the normal graded membrane responses and the spikes induced by procaine, tetraethylammonium, or barium. The inhibition is maintained throughout exposure to hypertonic solutions prepared by addition of impermeant solutes such as NaCl, sucrose, or Tris-propionate, but is reversible on their withdrawal. In the presence of permeant solutes such as glycerol or acetamide, the inhibition is transient. In both cases the onset of inhibition of the depolarizing Ca electrogenesis is correlated with shrinkage of the fiber. In the case of permeant solutes, the time course of recovery of the graded responses or the spikes follows the recovery of the fiber volume. Changes in the passive electrical characteristics of the fibers due to hypertonic solutions were unrelated to the blockade of membrane Ca activation. The current-voltage relationship in hypertonic sollution revealed no increase in depolarizing K activation. Inhibition of the graded membrane responses and spikes appears to be associated with depression of Ca conductance. Hypertonic solutions might affect the activation of Ca conductance through reduction of the electric field generated by fixed negative surface charges and/or morphological changes in the T tubules. Membrane depolarization elicited little or no tension in 2.0 T solutions while caffeine contracture (10 mM) with an ampliture of 76% of the maximal contractile ability could still be elicited. This indicates that direct effects of hypertonic solutions on the contractile apparatus were not responsible for loss of tension. The latter is attributed to the inhibition of the transmembrane Ca currents.

Acetamides↗
PubMed1976

A comparison of effects of SKF 525-A and procaine on excitation-contraction coupling in single crayfish muscle fibers.

The effects of beta-diethylaminoethyldiphenylpropylacetate hydrochloride (SKF 525-A) on excitation-contraction coupling and Ca-dependent electrogenesis are compared to those of procaine. At pH 7.2, SKF 525-A and procaine occur essentially (greater that 97%) as a free base and as a cation, respectively. At this pH, SKF 525-A elicited tension development, blocked K-induced contractures and the K-induced repriming of caffeine contractions, potentiated caffeine-induced tensions, inhibited the procaine-induced spikes and twitches and, depending on the concentration, either potentiated (25-50 muM) or depressed (greater than 100 muM) the tensions associated with the graded membrane electrogenesis. At the same pH, procaine blocked the contractions elicited by SKF 525-A, by high K media, by the graded electrogenesis and by caffeine, and converted the graded membrane responses into all-or-none spikes. It is proposed that SKF 525-A as a free base 1) inhibits membrane Ca activation more effectively than it depresses K conductance and 2) is synergistic with caffeine in reducing the effectiveness of Ca sequestration by the sarcoplasmic reticulum. Procaine as a cationic molecule is thought to depress K activation more than Ca activation during depolarization and to block the release of Ca ions from the sarcoplasmic reticulum.

Animals↗