Potassium Currents in Freshly Dissociated Uterine Myocytes from Nonpregnant and Late-Pregnant Rats

In freshly dissociated uterine myocytes, the outward current is carried by K(+) through channels highly selective for K(+). Typically, nonpregnant myocytes have rather noisy K(+) currents; half of them also have a fast-inactivating transient outward current (I(TO)). In contrast, the current records are not noisy in late pregnant myocytes, and I(TO) densities are low. The whole-cell I(K) of nonpregnant myocytes respond strongly to changes in [Ca(2+)](o) or changes in [Ca(2+)](i) caused by photolysis of caged Ca(2+) compounds, nitr 5 or DM-nitrophene, but that of late-pregnant myocytes respond weakly or not at all. The Ca(2+) insensitivity of the latter is present before any exposure to dissociating enzymes. By holding at −80, −40, or 0 mV and digital subtractions, the whole-cell I(K) of each type of myocyte can be separated into one noninactivating and two inactivating components with half-inactivation at approximately −61 and −22 mV. The noninactivating components, which consist mainly of iberiotoxin-susceptible large-conductance Ca(2+)-activated K(+) currents, are half-activated at 39 mV in nonpregnant myocytes, but at 63 mV in late-pregnant myocytes. In detached membrane patches from the latter, identified 139 pS, Ca(2+)-sensitive K(+) channels also have a half-open probability at 68 mV, and are less sensitive to Ca(2+) than similar channels in taenia coli myocytes. Ca(2+)-activated K(+) currents, susceptible to tetraethylammonium, charybdotoxin, and iberiotoxin contribute 30–35% of the total I(K) in nonpregnant myocytes, but <20% in late-pregnant myocytes. Dendrotoxin-susceptible, small-conductance delayed rectifier currents are not seen in nonpregnant myocytes, but contribute ∼20% of total I(K) in late-pregnant myocytes. Thus, in late-pregnancy, myometrial excitability is increased by changes in K(+) currents that include a suppression of the I(TO), a redistribution of I(K) expression from large-conductance Ca(2+)-activated channels to smaller-conductance delayed rectifier channels, a lowered Ca(2+) sensitivity, and a positive shift of the activation of some large-conductance Ca(2+)-activated channels.