The role of the electrogenic sodium pump in the potassium relaxation of the rabbit ear artery.

1. The mechanism of the potassium-induced relaxation of contracted vascular smooth muscle has been studied in helical strips of rabbit ear artery by recording isometric tension and membrane potential. The arteries were stimulated with a standard concentration of 2 x10(-8) M noradrenaline producing about 20% of the maximal contractile response to noradrenaline. 2. At K+ concentrations between 1.2 and 20.0 mM, a positive correlation was found between [K+]0 and the contractile response to noradrenaline, i.e. increasing [K+]0 enhanced the effect of noradrenaline. However, when noradrenaline was added after a 10 min exposure to reduced [K+]0 (1.2 mM) and [K+]0 was then increased to 5.9 mM after the tension had reached a plateau, a relaxation of about 50% occurred instead of the expected increase in tension. The relaxation was preceded by a membrane hyperpolarization of about 8 mV. 3. A biphasic change of both membrane potential and tension resulted when, after exposure of arterial strips to 1.2 mM K+ and stimulation with noradrenaline, [K+]0 was increased to 20.0 mM: hyperpolarization and relaxation developed faster than at 5.9 mM K+, but after 1 min the hyperpolarization changed to a depolarization followed by an increase in tension. 4. Ca2+-free solution and D 600 (an inhibitor of Ca2+ transmembrane flux) diminished, but did not abolish, the tension response to noradrenaline; in the presence of D 600, the hyperpolarization upon increasing [K+]0 after a previous exposure to 1.2 mM K+ was not affected, but a relaxation no longer occurred. 5. It is concluded that a) electrogenic ion transport causes the hyperpolarization that occurs when [K+]0 is increased after a period of exposure to low [K+]0; b) the hyperpolarization leads to relaxation by blocking the influx of extracellular Ca2+, but does not affect that component of the contractile response which is due to the release of intracellular Ca2+.