Basic hemodynamic studies on experimental coarctation of the aorta just beyond the left subclavian artery have revealed that hitherto unsuspected physical and physiologic factors are involved in creation of hypertension above a coarctation and in changes of pressure pulses below such a lesion. The effects are by no means explained by an increased resistance at the coarctation, as is generally believed. This communication analyzes the roles that changes in capacity and distensibility of the aortic compression chamber and increase in systolic discharge of the left ventricle play in the production of aortic hypertension, and discusses the physiologic compensations in blood flow by which an adequate return to the right heart is maintained despite extreme reduction in flow through the inferior cava. This communication also deals with the ways in which the pressure relations in the lower aorta and femoral artery are altered from the normal, emphasizing the relative shares that damping of the pulse wave and reduced input into the lower aorta play with different degrees of coarctation. The changing characteristics of the murmurs with progressive aortic constriction are also analyzed. The conclusion is reached that all the dynamic changes found in experimental and human coarctation are adequately explained without the assumption of accessory vasoconstriction through reflex or humoral agencies.