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  • acute renal failure  (2)
  • membrane currents  (2)
  • 1985-1989  (4)
  • 1975-1979
  • 1935-1939
  • 1890-1899
  • 1
    Electronic Resource
    Electronic Resource
    Effects of fatty acids on membrane currents in the squid giant axon (1987)
    Springer
    The journal of membrane biology 95 (1987), S. 113-120 
    Details
    ISSN: 1432-1424
    Keywords: fatty acids ; membrane currents ; membrane excitation ; 2-decenoic acid ; lateral motion ; squid axon
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Summary The effects of fatty acids on the ionic currents of the voltage-clamped squid giant axon were investigated using intracellular and extracellular application of the test substances. Fatty acids mainly suppress the Na current but have little effect on the K current. These effects are completely reversed after washing with control solution. The concentrations required to suppress the peak inward current by 50% and Hill number were determined for each fatty acid. ED50 decreased about 1/3 for each increase of one carbon atom. The standard free energy was −3.05 kJ mole−1 for CH2. The Hill number was 1.58 for 2-decenoic acid. The suppression effect of the fatty acids depends on the number of carbon atoms in the compounds and their chemical structure. Suppression of the Na current was clearly observed when the number of carbon atoms exceeded eight. When fatty acids of the same chain length were compared, 2-decenoic acid had strong inhibitory activity, but sebacic acid had no effect at all on the Na channel. The currents were fitted to equations similar to those proposed by Hodgkin and Huxley (J. Physiol. (London) 117:500–544, 1952) and the changes in the parameters of these equations in the presence of fatty acids were calculated. The curve of the steady-state activation parameter (m ∞) for the Na current against membrane potential and the time constant of activation ({ie113-1}) were shifted 20 mV in a depolarizing direction by the application of fatty acids. The time constant for inactivation ({ie113-2}) was almost no change by application of the fatty acids. The time constant for activation ({ie113-3}) of K current was shifted 20 mV in a depolarizing direction by the application of the fatty acids.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01869156
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  • 2
    Electronic Resource
    Electronic Resource
    Effects of arachidonic acid and the other long-chain fatty acids on the membrane currents in the squid giant axon (1988)
    Springer
    The journal of membrane biology 106 (1988), S. 141-147 
    Details
    ISSN: 1432-1424
    Keywords: arachidonic acid ; long-chain fatty acids ; membrane currents ; Na channel ; squid axon ; membrane excitation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Summary The effects of arachidonic acid and some other long-chain fatty acids on the ionic currents of the voltage-clamped squid giant axon were investigated using intracellular application of the test substances. The effects of these acids, which are usually insoluble in solution, were examined by using α-cyclodextrin as a solvent. α-cyclodextrin itself had no effect on the excitable membrane. Arachidonic acid mainly suppresses the Na current but has little effect on the K current. These effects are completely reversed after washing with control solution. The concentration required to suppress the peak inward current by 50% (ED50) was 0.18mm, which was 10 times larger than that of medium-chain fatty acids like 2-decenoic acid. The Hill number was 1.5 for arachidonic acid, which is almost the same value as for medium-chain fatty acids. This means that the mechanisms of the inhibition are similar in both long- and medium-chain fatty acids. When the long-chain fatty acids were compared, the efficacy of suppression of Na current was about the same value for arachidonic acid, docosatetraenoic acid and docosahexaenoic acid. The suppression effects of linoleic acid and linolenic acid on Na currents were one-third of that of arachidonic acid. Oleic acid had a small suppression effect and stearic acid had almost no effect on the Na current. The currents were fitted to equations similar to those proposed by Hodgkin and Huxley (Hodgkin, A.L., Huxley, A.F. (1952)J. Physiol (London) 117:500–544) and the change in the parameters of these equations in the presence of fatty acids were calculated. The curve of the steady-state activation parameter (m ∞) for the Na current against membrane potential and the time constant of activation (τ m ) were shifted 10 mV in a depolarizing direction by the application of fatty acids. The time constant for inactivation (τ h ) has almost unaffected by application of these fatty acids.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01871396
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  • 3
    Electronic Resource
    Electronic Resource
    Decreased Transport of p-Aminohippurate in Renal Basolateral Membranes Isolated from Rats with Acute Renal Failure (1989)
    Springer
    Pharmaceutical research 6 (1989), S. 954-957 
    Details
    ISSN: 1573-904X
    Keywords: p-aminohippurate ; tetraethylammonium ; transport ; basolateral membrane ; kidney ; acute renal failure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology
    Notes: Abstract Transport of D-glucose, p-aminohippurate (organic anion), and tetraethylammonium (organic cation) was studied in the renal basolateral membrane vesicles isolated from rats with acute renal failure (ARF). ARF was induced by a single injection of uranyl nitrate. Carrier-mediated transport of p-aminohippurate, estimated under anion–anion exchange condition, was significantly decreased in basolateral membrane vesicles isolated from ARF rats. In contrast, there were no significant differences in D-glucose and tetraethylammonium uptake between normal and ARF rats. When normal basolateral membrane vesicles were incubated in vitro with uranyl nitrate, no significant inhibition in p-aminohippurate uptake was observed. These results suggest that organic anion transport is decreased in renal basolateral membranes from ARF rats, and this transport dysfunction cannot be explained by the direct interaction of uranyl nitrate with the organic anion carrier.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1015993429458
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  • 4
    Electronic Resource
    Electronic Resource
    Urinary Excretion and Diuretic Action of Furosemide in Rats: Increased Response to the Urinary Excretion Rate of Furosemide in Rats with Acute Renal Failure (1988)
    Springer
    Pharmaceutical research 5 (1988), S. 699-703 
    Details
    ISSN: 1573-904X
    Keywords: furosemide ; acute renal failure ; increased response ; urinary excretion of furosemide ; dopamine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology
    Notes: Abstract A urinary excretion–response curve representing the urinary excretion rate of furosemide versus the urinary excretion rate of (Na+ + K+) was used to analyze furosemide action in rats with uranyl nitrate-induced acute renal failure (ARF) with and without dopamine coadministration. Urinary excretion of furosemide, but not its serum concentration, was the determinant for the diuretic action of furosemide. Increased diuretic response was observed in ARF rats, although the total diuretic response and urinary recovery of furosemide within 2 hr decreased. Dopamine enhanced furosemide-induced diuresis in ARF rats in terms of the total urine output and urinary electrolyte excretion, although the urinary excretion–response curves were not different. This enhancement by dopamine was found to be caused by the augmented urinary excretion of furosemide and the increased response to this drug in ARF rats. These findings suggest the contribution of decreased concentrating ability along the nephron and/or increased sensitivity of cells at the site of action to this drug.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1015951710204
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