Ca2+ influx inhibits voltage-dependent and augments Ca2+-dependent K+ currents in arterial myocytes |
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Authors: | Cox, Robert H. Petrou, Steven |
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Abstract: | These experiments were performed to determine the effects ofreducing Ca2+ influx(Cain) onK+ currents(IK) inmyocytes from rat small mesenteric arteries by1) adding externalCd2+ or2) lowering externalCa2+ to 0.2 mM. When measured froma holding potential (HP) of 20 mV(IK20),decreasing Cain decreasedIK at voltageswhere it was active (>0 mV). When measured from a HP of 60 mV(IK60),decreasing Cain increasedIK at voltagesbetween 30 and +20 mV but decreased IK at voltagesabove +40 mV. Difference currents(IK) weredetermined by digital subtraction of currents recorded under controlconditions from those obtained whenCain was decreased. At testvoltages up to 0 mV,IK60 exhibitedkinetics similar to controlIK60, with rapidactivation to a peak followed by slow inactivation. At 0 mV, peakIK60 averaged75 ± 13 pA (n = 8) withCd2+ and 120 ± 20 pA(n = 9) with lowCa2+ concentration. At testvoltages from 0 to +60 mV,IK60 always had an early positive peak phase, but its apparent "inactivation" increased with voltage and its steady value became negative above +20mV. At +60 mV, the initial peakIK60 averaged115 ± 18 pA with Cd2+ and 187 ± 34 pA with low Ca2+. With 10 mM pipette BAPTA, Cd2+ produced asmall inhibition ofIK20 but stillincreased IK60 between 30 and +10 mV. InCa2+-free external solution,Cd2+ only decreased bothIK20 andIK60. In thepresence of iberiotoxin (100 nM) to inhibitCa2+-activatedK+ channels(KCa),Cd2+ increasedIK60 at allvoltages positive to 30 mV while BAY K 8644 (1 µM) decreasedIK60. Theseresults suggest that Cain, through L-type Ca2+ channels and perhapsother pathways, increases KCa(i.e., IK20) and decreases voltage-dependent K+currents in this tissue. This effect could contribute to membrane depolarization and force maintenance. |
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