Blood flow control reflects dynamic, integrated changes in the diameter of vessels that comprise resistance networks. Vasoconstriction and vasodilation can travel rapidly along the vessel wall via the conduction of electrical signals between endothelial and/or smooth muscle cells through gap junctions. Within the hamster cheek pouch, these conducted responses reflect complementary mechanisms for co-ordinating both increases and decreases in arteriolar diameter. In the hamster retractor muscle, vasodilation also conducts along arterioles and into feed arteries, yet vasoconstriction appears constrained to the site(s) of smooth muscle activation. Thus, mechanisms for co-ordinating vasomotor control in resistance networks can vary between tissues that differ in structure and function. The resistance vessels of the retractor (and other skeletal) muscle are richly innervated by sympathetic nerves, which are absent from the cheek pouch. Propagation along sympathetic nerves rapidly co-ordinates smooth muscle cell contraction throughout the resistance network by releasing noradrenaline along the innervation pathway. Passive extension of the retractor muscle activates periarteriolar sympathetic nerves. This activity propagates antidromically into feed arteries and may complement the central (autonomic) vasoconstrictor response to exercise. In a reciprocal manner, muscle contraction evokes arteriolar dilation that is conducted (i.e. 'ascends') into feed arteries and may thereby counteract sympathetic vasoconstriction. With feed arteries anatomically positioned to control blood flow into skeletal muscle, the integration of dilator and constrictor stimuli in these vessels is a key determinant of muscle blood flow during exercise.