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  • Calcium-activated potassium channels  (1)
  • vascular smooth muscle  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Pflügers Archiv 408 (1987), S. 417-419 
    ISSN: 1432-2013
    Keywords: Ca2+·currents ; K+ currents ; vascular smooth muscle ; rat aorta
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Ca2+ (ICa) and K+ (IK) currents were recorded in single cultured cells from rat aorta using the whole cell clamp technique with patch electrodes. ICa was detected at−30 mV, and at 20 mV it reached a peak in about 10 ms and decayed with a t1/2=50 ms. The mean maximum slope conductance (GCa) was 30 μS/cm2. IK was detected at−10 mV and at 20 mV reached its maximum with a t1/2=12 ms. For IK, GK=200 μS/cm2. These channels can be activated during action potentials and play a role in the excitation and contraction of vascular smooth muscle cells.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Journal of bioenergetics and biomembranes 23 (1991), S. 561-576 
    ISSN: 1573-6881
    Keywords: Calcium-activated potassium channels ; modulation ; metabolic regulation ; neurotransmitters ; hormones ; lipids ; nucleotides
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Physics
    Notes: Abstract Calcium-activated potassium (KCa) channels are highly modulated by a large spectrum of metabolites. Neurotransmitters, hormones, lipids, and nucleotides are capable of activating and/or inhibiting KCa channels. Studies from the last few years have shown that metabolites modulate the activity of KCa channels via: (1) a change in the affinity of the channel for Ca2+ (K1/2 is modified), (2) a parallel shift in the voltage axis of the acitvation curves, or (3) a change in the slope (effective valence) of the voltage dependence curve. The shift of the voltage dependence curve can be a direct consequence of the change in the affinity for Ca2+. Recently, the mechanistic steps involved in the modulation of KCa channels are being uncovered. Some interactions may be direct on KCa channels and others may be mediated via G-proteins, second messengers, or phosphorylation. The information given in this review highlights the possibility that KCa channels can be activated or inhibited by metabolites without a change in the intracellular Ca2+ concentration.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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