We examined the influence of stellate ganglion stimulation, hypoxia, and the infusion of norepinephrine, PGF2alpha, serotonin, and histamine on the longitudinal distribution of vascular resistance and intravascular pressures in an isolated left lower lobe of the dog lung using the low-viscosity bolus technique. Sympathetic stimulation, norepinephrine, serotonin, PGF2alpha, and hypoxia increased total pulmonary vascular resistance by increasing the resistance, primarily on the arterial or upstream side of the volume midpoint, whereas histamine increased the resistance near the venous end of the lobar vascular bed. Hypoxia increased the volume upstream from the site of maximum resistance, suggesting that the larger lobar arteries were distended by the elevated lobar artery pressure. Sympathetic stimulation, norepinephrine, PGF2alpha, and serotonin, on the other hand, had little effect on the volume upstream from the maximum resistance, suggesting that these vasomotor stimuli prevented distension of the larger arteries.