Steady-state effects of extracellular potassium concentration on vascular smooth muscle reactivity.

Abstract

Helical strips cut from small arteries taken from rabbit skeletal muscle were used to determine the steady-state effects of extracellular potassium concentration ([K]o) on the reactivity to epinephrine or norepinephrine. It was found that reactivity observed under the usual steady-state conditions (termed "usual reactivity") was depressed as steady-state [K]o was reduced from 8 to 1 mM. This depression reflected concurrent changes in two components of contraction: 1) a positive component (evaluated as reactivity during brief exposure to 10(-6) M ouabain) decreased when steady-state [K]o was reduced below approximately 5 mM, and 2) a negative component (evaluated indirectly as enhancement of reactivity produced by 10(-6) M ouabain) increased to a peak when steady-state [K]o was reduced from 8 to approximately 4-5 mM and decreased below this peak when steady-state [K]o was reduced below approximately 4-5 mM. It was also found that the magnitude of a reserve ouabain-sensitive negative component (demonstrated by abruptly increasing [K]o to 10.18 mM) increased from a minimum to a maximum level when steady-state [K]o was reduced from 6 to 3 mM. It is suggested that the effects of [K]o on the positive component of contraction, defined earlier as contractility, primarily involve some factor(s) other than transmembrane potential, whereas the effects on the negative component involve transmembrane potential exclusively and, in particular, the electrogenic potential. The latter suggestion constitutes the basis for use of the term electrogenesis in reference to this negative component.