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E Ríos

Publications and source records attributed to E Ríos.

At least 73 records · Page 4Linked to original sources
PubMed1988

Effects of extracellular calcium on calcium movements of excitation-contraction coupling in frog skeletal muscle fibres.

1. The effect of low extracellular free calcium ion concentration ([Ca2+]o) on the transient changes in cytoplasmic [Ca2+] associated with membrane depolarization (Ca2+ transients) was studied on single cut skeletal muscle fibres of the frog, voltage clamped in a double-Vaseline-gap chamber. The Ca2+ transients were monitored with the dye Antipyrylazo III diffused intracellularly. 2. The Ca2+ transients were substantially reduced in external salines with low [Ca2+] (10(-5) M or less and Mg2+ substituted for Ca2+). This decrease was more noticeable at late times during 100 ms or longer depolarizing pulses. 3. The rates of the processes that remove Ca2+ from the myoplasmic solution were not altered by the low [Ca2+]o. This implies that the input flux of Ca2+ into the myoplasm was reduced. 4. The Ca2+ input flux, equal to release flux from the sarcoplasmic reticulum (SR) plus Ca2+ influx via the T-tubule membrane Ca2+ channel, was derived from the Ca2+ transient. In low [Ca2+]o the peak input flux was reduced by 45% (n = 16 fibres) and decayed more rapidly during a depolarizing pulse. 5. The reduction in Ca2+ influx via the T-tubule membrane Ca2+ channel due to the reduced [Ca2+]o could not account for more than 5% of the reduction in Ca2- input flux, which was thus interpreted as an actual reduction of release from the SR. 6. The inward (T-tubular) Ca2+ current was not associated with this effect of extracellular Ca2+ as the effect was voltage independent at high intracellular voltages at which the Ca2+ inward current was strongly voltage dependent. 7. Low [Ca2+]o made Ca2+ release more readily inactivatable; the effect of low [Ca2-]o is best described as a left shift by 29 mV of the 'inactivation curve' of Ca2+ release, relating peak release flux to membrane holding potential. 8. The reduction of Ca2+ release by low [Ca2+]o was not accompanied by changes in the voltage dependence of Ca2+ release or in the threshold voltage for just-detectable release. 9. The results are consistent with a primary effect of Ca2+ on the T-tubular-membrane voltage sensor of excitation-contraction coupling.

Animals↗
PubMed1988

Voltage sensors of the frog skeletal muscle membrane require calcium to function in excitation-contraction coupling.

1. Intramembrane charge movements and changes in intracellular Ca2+ concentration (Ca2+ transients) elicited by pulse depolarization were measured in frog fast twitch cut muscle fibres under voltage clamp. 2. Extracellular solutions with very low [Ca2+] and 2 mM-Mg2+ , shown in the previous paper to reduce Ca2+ release from the sarcoplasmic reticulum (SR), were found to cause two changes in charge movement: (a) a decrease (-12 nC/microF) in the charge that moves during depolarizing pulses from -90 to 0 mV, termed here 'charge 1'; (b) an increase (+7 nC/microF) in the charge moved by hyperpolarizing pulses from -90 to -180 mV, termed 'charge 2'. 3. The increase in charge moved by hyperpolarizing pulses was correlated (r = 0.64) with the decrease in charge moved by depolarizing pulses and both were correlated with the inhibition of Ca2+ release recorded in the same fibres. 4. The low Ca2+ solutions caused a shift to more negative voltages of the dependence relating charge movement and holding potential (VH). This shift is of similar magnitude (about 22 mV) and direction as the shift in the curve relating Ca2+ release flux to VH (previous paper). 5. In solutions with normal [Ca2+] a conditioning depolarization to 0 mV, of 2 s duration, placed 100 ms before a test pulse from -70 to 0 mV, reduced by 30% the amount of charge displaced by the test pulse. Conditioning pulses of 1 s or less caused potentiation of charge movement by up to 30%. 6. In low Ca2+ solutions, reduction of charge was observed at all durations of the conditioning pulse. The duration for half-inhibition was near 200 ms. 7. An extracellular solution with no metal cations caused a more radical inhibition than the low Ca2+ solutions that contained Mg2+. The inhibition of Ca2+ release was essentially complete (90-100%). The charge moved by a pulse to 0 mV was reduced by 20 nC/microF and the charge moved by a pulse to -170 mV increased 8 nC/microF. This shows that Mg2+ supports excitation-contraction (E-C) coupling to some extent. 8. A state model of the voltage sensor of E-C coupling explains qualitatively the observations in both papers.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1986

The removal of myoplasmic free calcium following calcium release in frog skeletal muscle.

Transient changes in intracellular free calcium concentration (delta [Ca2+]) in response to pulse depolarizations were monitored in isolated segments of single frog skeletal muscle fibres cut at both ends and voltage clamped at a holding potential of -90 mV in a double-Vaseline-gap chamber. Calcium transients were monitored optically using the metallochromic indicator dye Antipyrylazo III (APIII), which entered the fibre by diffusion from the solution applied to the cut ends. Optical artifacts due to fibre movement were minimized or eliminated by stretching the fibres to sarcomere lengths at which there was little or no overlap of thick and thin contractile filaments. Remaining movement-independent optical changes intrinsic to the fibre and unrelated to the dye were monitored at 850 nm, where free and dye-bound APIII have no absorbance. These 850 nm signals scaled by lambda -1.2 were used to remove intrinsic components from the signals at 700 or 720 nm, wave-lengths at which the APIII absorbance increases when calcium is bound. The corrected 700 or 720 nm signals were used to calculate delta [Ca2+]. The decay of delta [Ca2+] following fibre repolarization at the termination of a depolarizing pulse was well described by a single exponential plus a constant. The exponential rate constant for the decay of delta [Ca2+] decreased and the final 'steady' level that delta [Ca2+] appeared to be approaching increased with increasing amplitude and/or duration of the depolarizing pulse. Both the decreasing decay rate and the build up of the 'steady' level can be accounted for using a two-component model for the removal of free calcium from the myoplasm. One component consists of a set number of a single type of saturable calcium binding site in the myoplasm. The second component is a non-saturable, first-order uptake mechanism operating in parallel with the saturable binding sites. The removal model parameter values were adjusted to fit simultaneously the decay of delta [Ca2+] after pulses of various amplitudes and durations in a given fibre. The basic procedure was to track delta [Ca2+] during each pulse when an undetermined calcium release was occurring, but to calculate the decay of delta [Ca2+] starting 14 ms after repolarization when release was assumed to be negligible. After appropriate selection of parameter values, the model reproduced most aspects of the decay of delta [Ca2+].(ABSTRACT TRUNCATED AT 400 WORDS)

Actin Cytoskeleton↗
PubMed1981

Stoichiometry of the reactions of calcium with the metallochromic indicator dyes antipyrylazo III and arsenazo III.

A method for determining the stoichiometry of one-product reactions involving a metal ion and an organic ligand is presented and applied to the reactions of calcium and magnesium with the metallochromic dyes Antipyrylazo III and Arsenazo III. The method consists of fitting titration data, obtained in solutions buffered for the metal, with theoretical functions that include: (a) the dependence of product concentration on the concentration of both reactants, (b) the relationship between metal ion concentration and total amount added in the presence of the buffer, and (c) a correction for the amount of metal ion that binds to the organic ligand. It is shown that the products of the reactions of Antipyrylazo III with calcium and magnesium are CaD2 and MgD, respectively. The product formed between calcium and Arsenazo III at [Ca2+] over 20 microM is CaD2, other products accumulating at lower [Ca2+]. The kinetics of the Antipyrylazo III:Ca reaction are rapid under conditions in which this dye has been applied to measure calcium transients in skeletal muscle fibers. The present results provide a calibration for previous studies with Antipyrylazo III in muscle fibers.

Absorption↗
PubMed1979

Calcium transients and intramembrane charge movement in skeletal muscle fibres.

Myoplasmic calcium transients in response to pulse depolarisations have been monitored using the dye antipyralazo III, which provides a linear measure of the change in cytoplasmic free calcium concentration. Intramembrane charge movements were recorded simultaneously with the calcium transients. Except for its initial phase, the calcium transient during each pulse closely followed the time course expected for calcium redistribution between three intracellular compartments with time-independent flux coefficients. The time at which the flux coefficients attained their steady values occurred just after the intramembrane charge movement had been completed. This is the required sequence if charge movement were to control one or more coefficients f or calcium fluxes across the sarcoplasmic reliculum membrane.

Journal Article↗
PubMedDate not supplied

[Lead exposure and its effects on child health].

Childhood lead poisoning is a man-made disease whose magnitude has not yet been measured in Chile. In the U.S.A. it has been estimated that 4 percent of children have elevated blood lead levels and that among poor black children, this rate is as high as 18 percent. The main sources of symptomatic lead poisoning are lead-based paint used in interior and exterior house surfaces, airborne lead from leaded gasoline and industrial emissions. Lead can be transferred from any source to soil and dust. Other sources of lead are contaminated food and water, occupational sources, and lead glazed pottery. Neurological symptoms (hyperactivity, distractibility, lower intellectual development), psychological difficulties (behavioral deficits), hematologic abnormalities (reduction in the biosynthesis of heme, anemia), and metabolic changes (reduction in concentration of 1-25 dihydroxy vitamin D and in the metabolism of erythrocyte pyrimidine) have been shown to occur in lead poisoning. Recent data suggests that prenatal exposure to lead my be related to minor congenital abnormalities, tumors of the kidney, and growth abnormalities.

Air Pollution↗