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Fig. 1. Effect of OA on the voltage-activated L-type current carried by barium in
sea bass ventricular myocytes. (A,B) The current was elicited by a step in
membrane potential to 0 mV from a holding potential of –80 mV (insert)
during 300 ms (A) at 1/20 Hz. Superimposed traces show responses of a cell in
control solution, after 5 min exposure to 30 µmol l–1 OA
(A) and 3 µmol l–1 nifedipine (B) (capacitance=40.71 pF).
(C) Time course of the inhibitory effect of OA on the peak
IBa,L. Peak currents were normalised to their initial peak
current recorded at t=0 min of perfusion and are expressed as mean
± s.e.m. Black crosses, control perfusion without OA (N=11);
green squares, yellow triangles, red diamonds and blue circles, OA
concentrations of 5 (N=3), 10 (N=4), 30 (N=10) and
100 µmol l–1 (N=6), respectively. Significant
differences between control and the different OA concentrations are indicated
(*P<0.05, **P<0.01). (D) Concentration dependence of
inhibition by OA on IBa,L after 5 min of perfusion. The
number of cells treated with OA at 5, 10, 30 and 100 µmol
l–1 is 3, 4, 10 and 6, respectively. The line was obtained by
fitting data to the Hill equation (see Materials and methods), which gave an
IC50 of 12.49±0.27 µmol l–1 and a Hill
factor of 1.97±0.07. Values are mean ± s.e.m. Dissimilar letters
indicated a significant difference (P<0.05) of
IBa,L diminution between the different OA
concentrations.
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