ISSN:
1432-2013
Keywords:
Key words Ruthenium red
;
Smooth muscle
;
Ca2+-dependent K+ channel
;
Ca2+ channel
;
Ryanodine
;
Urinary bladder
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Abstract Three major ionic currents, Ca2+-dependent K+ current (I K-Ca), delayed rectifier type K+ current (I kd) and Ca2+ current (I Ca), were activated by depolarization under whole-cell clamp in single smooth muscle cells isolated from guinea-pig urinary bladder. Externally applied ruthenium red (RuR) reduced the amplitude of I K-Ca and I Ca at 0 mV (IC50 values were 4.2 and 5.6 μM, respectively), but did not affect I Kd. Spontaneous transient outward currents (STOCs) and caffeine-induced outward currents (I caf) at –30 mV were reduced by external 10 μM RuR. When 10 μM RuR was added to the pipette solution, I K-Ca during depolarization, STOCs and I caf significantly decreased with time. RuR did not change the unitary current amplitude of the large-conductance Ca2+-dependent K+ (BK) channels, but reduced the open probability of the channel under excised patch-clamp recording mode. RuR reduced the channel activity more effectively from the cytosolic face than from the other. This inhibition decreased when the cytosolic Ca2+ concentration was increased. These results indicate that RuR blocks BK and Ca2+ channels in urinary bladder smooth muscle cells. The decrease in I K-Ca, STOCs and I caf by RuR is attributable to the direct inhibition of BK channel activity, probably in addition to the inhibition of Ca2+ release from storage sites. The direct inhibition of BK channel activity by RuR may be related to the interaction of RuR with the Ca2+-binding sites of the channel protein.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/s004240050565
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