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The effects of halothane (0.75% and 1.5%) and isoflurane (2.6%) on macroscopic Ca2+ and K+ channel currents (ICa and IK, respectively) were investigated in voltage-clamped vascular muscle cells from the canine coronary artery. Single coronary arterial cells were dialyzed with K+ glutamate solution and superfused with Tyrode's solution for measurement of IK (n = 45). Stepwise depolarization from a holding potential of -60 mV to beyond -30 mV elicited an outward, slowly inactivating IK that had a macroscopic slope conductance of 18 nS. IK was reduced 75% by 10 mM 4-aminopyridine, a K+ channel antagonist. Compared to 4-aminopyridine, halothane at 0.75% and 1.5% reduced peak IK amplitude only by 14 +/- 2% and 36 +/- 3%, respectively. At approximately equianesthetic concentrations, 2.6% isoflurane suppressed IK less than did 1.5% halothane, reducing peak amplitude by 15 +/- 3%. In other sets of experiments, cells were dialyzed with 120 Cs(+)-glutamate solution and superfused with 10 mM BaCl2 or CaCl2 solutions to isolate ICa (n = 39) pharmacologically. Under these conditions, progressive depolarizing steps from -60 mV elicited a small inward current, which was potentiated 3.4-fold by equimolar substitution of Ba2+ for Ca2+ in the external solution and was blocked by 1 microM nifedipine. This inward current, which resembled L-type ICa, was blocked 37 +/- 4% and 70 +/- 4% in the presence of 0.75% and 1.5% halothane, respectively. Isoflurane (2.6%) also decreased ICa by 55 +/- 5%. It appears that while halothane and isoflurane suppress both IK and ICa, these anesthetics preferentially reduce ICa.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of Halothane and Isoflurane on Calcium and Potassium Channel Currents in Canine Coronary Arterial Cells