Vasodilatation is obligatory for contraction-induced hyperaemia in canine skeletal muscle.

Abstract

There is a rapid increase in blood flow to active skeletal muscle with the onset of exercise, but the mechanism(s) eliciting this increase remains elusive. We hypothesized that the rapid increase in blood flow to active skeletal muscle with the onset of exercise is attributable to vasodilatation as a consequence of smooth muscle hyperpolarization. To test this hypothesis we examined the blood flow response to a brief tetanic contraction in which potassium (K(+)) was infused intra-arterially to elevate the [K(+)](o) and clamp the smooth muscle membrane potential within the skeletal muscle vascular bed. In six anaesthetized beagle dogs control contractions increased hindlimb blood flow by 97 +/- 14 ml min(-1). During K(+) infusion the hyperaemic response to contraction was 8 +/- 3 ml min(-1). Since the hindlimb blood flow was reduced during K(+) infusion, a similar reduction in baseline blood flow was produced with phenylephrine infusion. During phenylephrine infusion the hyperaemic response to contraction was preserved (89 +/- 23 ml min(-1)). Recovery contractions performed after the discontinuation of the K(+) infusion elicited blood flow responses similar to control (100 +/- 11 ml min(-1)). In a separate experimental protocol using the isolated gastrocnemius muscle of mongrel dogs (n= 6) K(+) infusion did not alter force production by the skeletal muscle. Our data indicate that in the absence of vasodilatation, there is virtually no change in blood flow. One implication of this finding is that the muscle pump cannot be responsible for the initial contraction-induced hyperaemia. We conclude that the increase in blood flow immediately following a single muscle contraction is due to vasodilatation, presumably as a consequence of smooth muscle hyperpolarization.