Is Potassium Responsible for Contraction-Induced Hyperemia?

Abstract

One theory that has been proposed to explain exercise hyperemia is that vasodilation in contracting skeletal muscle is due to rapid accumulation of K+ in the interstitium. Previous descriptive studies have shown that the time course of increased [K+] in venous blood following muscle contraction correlates well with the observed time course of changes in blood flow. Interestingly, the vascular smooth muscle response to K+ is biphasic, with hyperpolarization and dilation at low concentrations and depolarization and constriction at high concentrations. Theoretically, it should be possible to infuse K+ at a concentration which would not change the smooth muscle membrane potential nor blood flow. We reasoned that if K+ release from muscle plays a substantive role in contraction-induced hyperemia, imposing a contraction during K+ infusion would further elevate interstitial [K+] which would cause constriction. PURPOSE We hypothesized that contraction during K+ infusion would further increase the interstitial [K+] causing vasoconstriction. METHODS In anesthetized dogs (n=5) hindlimb blood flow was monitored with transit time ultrasonic flowprobes placed around the external iliac arteries. A femoral artery catheter was placed for K+infusion. Brief tetanic contractions were evoked by stimulation of the sciatic nerve for 1 sec (50Hz, 0.2ms). RESULTS As anticipated, intraarterial infusion of low doses of K+ produced dilation, high doses produced constriction, and intermediate doses produced no change in blood flow. Under control conditions, a single titanic contraction increased hindlimb blood flow by 113±15 ml/min. However, at an intermediate infusion rate of K+ that did not change blood flow from the baseline, a single contraction evoked an increase in hindlimb blood flow of 43±19 ml/min. In none of the experiments was vasoconstriction observed in response to contraction. CONCLUSIONS These data do not support the notion that K+ is an important contributor to vasodilation evoked by muscle contraction. Supported by NIH and VA Medical Research.