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  • 1
    ISSN: 1432-2013
    Keywords: Excitation-contraction coupling ; Cell calcium ; Cardiac muscle ; Thyroid hormone ; Aequorin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The purpose of this study was to determine the influence of thyroid hormone on tension development and the intracellular calcium transient in mammalian ventricular muscle. A hyperthyroid (H) state was induced in ferrets by subcutaneous injection ofl-thyroxine, 0.3 mg/kg daily, for 2–3 weeks. One-half of the age matched control group (C) were injected with vehicle. Aequorin was loaded into the cells of ferret papillary muscles by a chemical procedure. The muscles were stimulated at 0.33 Hz and isometric tension and the calcium transient were simultaneously recorded at 30°C. Peak isometric tension in mN/mm2 (±SD) was 15.4±7.2 and 16.2±7.9 for C (n=8) and H (n=9) respectively. The time to peak tension and time to 80% relaxation from peak of tension were reduced by 22% and 28% respectively in H compared to C. After stimulation, the calcium transient reached a maximum in 56±6 ms in C and in 47±5 ms in H. The time to 80% decay of the peak calcium transient was 95±8 ms and 68±5 ms for C and H respectively. The ratio of the aequorin luminescence at the peak of the calcium transient over the calculated maximum luminescence,L max, were compared and they were not different. At 22°C Log (L/L max) was −3.3±0.1 in C (n=4) and −3.4±0.3 in H (n=3). These results indicate that the thyroid state influences the time course of the calcium transient and are consistent with the abbreviation in the duration of contraction that is observed in the hyperthyroid state.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-2013
    Keywords: Aequorin ; Calcium indicators ; Cyanide ; Hypoxia ; Ferret ; Oxidative phosphorylation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We used the bioluminescent Ca2+ indicator, aequorin to record intracellular calcium transients during reoxygenation of hypoxic ferret ventricular muscle in order to determine whether alterations in the amplitude and time course of isometric contraction are emdiated by changes in [Ca2+]i. Papillary muscles ≤1 mm in diameter were removed from the hearts of male ferrets and perfused with a bicarbonate-buffered physiologic salt solution at 30°C. Muscles were stimulated to contract isometrically at 0.33 Hz and were loaded with aequorin by a chemical procedure. Hypoxia was induced by changing the gas mixture bubbling the perfusate to 95% N2, 5% CO2; reoxygenation was accomplished by switching the gas mixture to 95% O2, 5% CO2. Hypoxia produced a decrease in peak Ca2+ and tension that was reversed by reoxygenation. However, the effects on tension of changes in oxygenation were greater than expected from the degree of change in [Ca2+]i. The time courses of the Ca2+ transient and isometric twitch moved in opposite directions and were respectively prolonged/abbreviated by hypoxia and abbreviated/prolonged by reoxygenation. These results indicate that changes in the amplitude and time course of the isometric twitch induced by hypoxia and reoxygenation cannot be attributed alone to changes in intracellular Ca2+ availability and are caused in part by a significant decrease in the calcium sensitivity of the contractile apparatus.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    ISSN: 1573-6881
    Keywords: Potassium channels ; membrane proteins ; channel gating ; ion permeation ; mutagenesis ; channel structure ; shaker ; TEA ; charybdotoxin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Physics
    Notes: Abstract The voltage-activated K+ channels are members of an ion channel family that includes the voltage-activated Na+ and Ca2+ channels. These ion channels mediate the transmembrane ionic currents that are responsible for the electrical signals produced by cells. The recent cloning of numerous voltage-activated K+ channels has made it possible to combine molecular-genetic and biophysical methods to study K+ channel mechanisms. These mutagenesis-function studies are beginning to provide new information about the architecture of K+ channel proteins and how they form a voltage-gated, K+-selective pore.
    Type of Medium: Electronic Resource
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