Is the blood flow response to contraction attributable to potassium?

Release of potassium ions by skeletal muscle has been postulated as a plausible explanation for the marked hyperemia observed following muscle contraction. Seven mongrel dogs (22.4±1.7 kg), of either sex, were anesthetized and instrumented for measurement of arterial blood pressure and bilateral external iliac artery blood flow. Dogs were placed in the upright position and a brief (1s) tetanic muscle contraction was evoked via electrical stimulation of the cut sciatic nerve before/after blockade of both inward rectifying K + channels (barium) and Na + /K + pump (ouabain). Effective blockade was demonstrated by absence of a response to an intraarterial bolus of K + (20 mg). Nonspecific effects of K + blockade were tested by infusion of acetylcholine (0.5μg bolus). K + blockade reduced baseline blood flow from 148±36 to 95±14 ml/min. Thus, control measurements were taken during phenylephrine infusion to normalize baseline blood flows. Contraction elicited a 243±42 ml/min increase in blood flow and acetylcholine infusion increased blood flow by 427±80 ml/min. In the presence of barium and ouabain, responses were reduced to 147±28 and 259±52 ml/min, respectively. The proportional (39%) decrease in the hyperemic response to contraction and acetylcholine suggests that blockade of inward rectifying K + channels and Na + /K + pump inhibits vasodilation in a nonspecific manner, but does not selectively alter the blood flow response to contraction. Therefore, we conclude that K + ions released from skeletal muscle are not obligatory for the hyperemic response to a brief muscle contraction. This study was supported by NHLBI, VA Medical Research, and Croatian Ministry of Science, Education and Sports.