Abstract
The effect of K+ depolarization and agonists on the 86Rb+ efflux from rabbit ear artery has been investigated. K+ depolarization with 59 mM-K+ induces an increase of the 86Rb+ efflux rate, which is dependent on [Ca2+]o and is correlated with the concomitant force development. This effect is largely reduced by Ca2+ antagonists, such as D-600 and Mn2+. The residual increase of the 86Rb+ efflux rate is much smaller than that predicted by the constant-field equations. Stimulation with 10(-5) M-noradrenaline or 10(-4) M-histamine induces a biphasic increase of the efflux rate. The initial transient effect is reduced in low [Ca2+]o solutions, whereas the maintained component is largely independent of [Ca2+]o. Stimulation with noradrenaline during depolarization of the tissues with K+ induces, after a transient increase of the efflux rate, an inhibition of the K+-induced increase of the efflux rate. Both phases of the noradrenaline action are due to activation of alpha-adrenoreceptors. Exposure to Ca2+-free medium induces a progressive increase of the 86Rb+ efflux rate, which reaches a new steady-state value after about 60 min. Stimulation with noradrenaline after this 60 min exposure to Ca2+-free solution no longer induces a significant effect. Stimulation with noradrenaline after shorter exposures to Ca2+-free solution immediately increases the 86Rb+ efflux to a value close to the steady-state value obtained after prolonged exposure to Ca2+-free medium. Washing out the agonist has no effect on the rate constant. It will only return to its control value after exposure to solutions containing Ca2+. This recovery of the rate constant by external Ca2+ also occurs in the presence of 1 mM-Mn2+ in the perfusion fluid. On re-exposure of the tissues in the presence of 1 mM-Mn2+ to Ca2+-free solution the rate constant of the 86Rb+ efflux increases at once to the steady-state value observed in Ca2+-free solution. This increase proceeds gradually if the tissues have been re-exposed in the absence of Mn2+. It is concluded that K+ permeability might be regulated by [Ca2+]i and that this relationship can be affected by agonists. In order to explain the effects of Ca2+-free medium on the 86Rb+ efflux we have to assume that at very low values of [Ca2+]o and [Ca2+]i the membrane permeability for K+ is modified by a different mechanism.