Ionic regulation of peripheral vascular tone and its interaction with norepinephrine.

The effects of various concentrations of K+ (0, 0.5, 1, 2.5, 5, 7.5, 10, 20, and 40 mM) on the tone of femoral arterial strips of rabbit were studied. None of the concentrations of K+ produced relaxation of the arterial strips. Potassium in the concentrations of 10 mM and above produced a concentration dependent increase in the arterial tone. Potassium-induced contraction was dependent upon extracellular Ca++. Norepinephrine (NE) produced contraction in the absence of K+ but the norepinephrine-induced contraction increased with increasing concentration of K+ to a limit. Potassium in lower concentrations (8, 16, 32 mM) accelerated the rate of relaxation of norepinephrine-induced contraction. Verapamil in the concentration of 0.1, 0.5 and 1 microgram/ml produced a concentration dependent inhibition of K+-induced contraction and this inhibition was inversely proportional to the extracellular Ca++. Verapamil in the concentration of 0, 0.1, 0.2, 0.5, 1, 2, 4, 8, and 10 micrograms/ml produced a concentration dependent inhibition of norepinephrine (1 microgram/ml) and potassium (40 mM)-induced contraction. The concentration of verapamil (2 micrograms/ml) which produced 92% inhibition of K+-induced contraction, produced only 48% inhibition of norepinephrine-induced contraction. Even 10 micrograms/ml of verapamil could not block the effect of NE. These results suggest that potassium is not a vasodilator and that there is interaction between K+ and Ca++, and K+ and NE. Ca++ channel blocker has a differential effect on the K+ and NE-induced contraction.