When the vascular smooth muscle of arterioles relaxes in response to vasodilator metabolites whose release is caused by a decrease in the ratio of O2 supply to O2 demand of the tissue, resistance may diminish concomitantly in the small upstream arteries that feed these arterioles. The result is blood flow greater than that produced by arteriolar dilation alone. There are two possible mechanisms for this coordination of arterial and arteriolar dilation. First, the vasodilation in the microvessels may be propagated, and when dilation is initiated in the arterioles, it can propagate along the vessels from the arterioles back to the small arteries. Second, the metabolite-mediated dilation of the arterioles accelerates blood flow in the feeder arteries. This greater blood flow velocity increases the shear stress on the arterial endothelium, which in turn can induce flow-mediated vasodilation by release of one or more vasodilators (e.g., nitric oxide, prostacyclin, H2O2, epoxyeicosatrienoic acid).
Inthelegs,diseaseofthearterialwallscanleadtoobstructionofthearteriesandsymptoms,aconditioncalledintermittent claudication. Thesymptomsconsistoflegpainwhenthepersonwalksorclimbsstairs,andthepainisrelievedbyrest.Thediseaseiscalledthromboangiitis obliterans, anditappearsmostfrequentlyinmenwhoaresmokers.Withminimalwalking,theresistancevesselsbecomemaximallydilatedbylocalreleaseofmetabolites;whentheO2demandofthemusclesincreaseswithmorerapidwalking,bloodflowcannotincreasesufficientlytomeetthemuscleneedsforO2,andpaincausedbymuscleischemiaresults.
Extrinsic Control of Peripheral Blood Flow
Several regions in the cerebral medulla influence cardiovascular activity. Stimulation of the dorsal lateral medulla (pressor region) evokes vasoconstriction, cardiac acceleration, and enhanced myocardial contractility. Stimulation of cerebral centers caudal and ventromedial to the pressor region decreases arterial blood pressure. This depressor area exerts its effect by direct inhibition of spinal regions and by inhibition of the medullary pressor region. These areas are not true anatomical centers in which a discrete group of cells is discernible, but they constitute “physiological” centers.
The cerebrospinal vasoconstrictor regions are tonically active. Reflexes or humoral stimuli that enhance this activity increase the frequency of impulses that reach the terminal neural branches to the vessels. A constrictor neurohumor (norepinephrine) is released at the terminals to elicit a constrictive α-adrenergic effect on the resistance vessels. Inhibition of the vasoconstrictor areas diminishes the impulse frequency in the efferent nerve fibers, and vasodilation results. Thus neural regulation of the peripheral circulation is achieved mainly by alteration in the impulse frequency in the sympathetic nerves to the blood vessels. Surgical section of the sympathetic nerves to an extremity abolishes sympathetic vascular tone and thereby increases blood flow to that limb. With time, vascular tone is regained by an increase in basal (intrinsic) tone.
Both the pressor and depressor regions may undergo rhythmic changes in tonic activity that are manifested as oscillations in arterial pressure. Some rhythmic changes (Traube-Hering waves) occur at the frequency of respiration and are caused by a cyclic fluctuation in sympathetic impulses to the resistance vessels. Other fluctuations in sympathetic activity (Mayer waves) occur at a frequency lower than that of respiration.