The effects of the agonist enantiomer S(−)Bay K 8644 on gating charge of L-type Ca channels were studied in single ventricular myocytes. From a holding potential (V h) of −40 mV, saturating (250 nM) S(−)Bay K shifted the half-distribution voltage of the activation charge (Q1) vs. V curve −7.5 ± 0.8 mV, almost identical to the shift produced in the Ba conductance vs. V curve (−7.7 ± 2 mV). The maximum Q1 was reduced by 1.7 ± 0.2 nC/µF, whereas Q2 (charge moved in inactivated channels) was increased in a similar amount (1.4 ± 0.4 nC/µF). The steady-state availability curves for Q1, Q2, and Ba current showed almost identical negative shifts of −14.8 ± 1.7 mV, −18.6 ± 5.8 mV, and −15.2 ± 2.7 mV, respectively. The effects of the antagonist enantiomer R(+)BayK 8644 were also studied, the Q1 vs. V curve was not significantly shifted, but Q1 max (V h = −40 mV) was reduced and the Q1 availability curve shifted by −24.6 ± 1.2 mV. We concluded that: a) the left shift in the Q1 vs. V activation curve produced by S(−)BayK is a purely agonistic effect; b) S(−)BayK induced a significantly larger negative shift in the availability curve than in the Q1 vs. V relation, consistent with a direct promotion of inactivation; c) as expected for a more potent antagonist, R(+)Bay K induced a significantly larger negative shift in the availability curve than did S(−) Bay K.
The Journal of Membrane Biology – Springer Journals
Published: Jun 1, 2003
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