The possibility of changes in the adrenergic innervation of blood vessels in experimental hypertension was investigated by measuring arterial norepinephrine content, neuronal uptake of norepinephrine, and the neurogenic contractile response in rabbits made hypertensive by partial constriction of the abdominal aorta proximal to the kidneys. Two to 3 weeks after surgery, norepinephrine content was increased in the arteries above the ligature, where arterial blood pressure was increased, but not in the arteries below the ligature, where arterial blood pressure was normal, in the heart, or in the veins. Neuronal norepinephrine uptake per unit length of vessel and the neurogenic contractile response increased with the rise in arterial blood pressure. The neurogenic contractile response can be taken as an indication of an increase in transmitter release. The results taken together suggest an increase in the function and possibly the amount of the adrenergic neuroneal terminal in hypertension. Since the distributions of the changes in the adrenergic innervation and the increases in smooth muscle cell proliferation in hypertension are similar, these two processes may be interrelated.

Vessel dimensions and characteristic responses to norepinephrine were measured in various arteries and veins of the rabbit made hypertensive by partial constriction of the upper abdominal aorta. The ear, radial, and basilar arteries taken from the circulation proximal to the ligature (the hypertensive arteries) were thickened in proportion to the rise is arterial blood pressure. The water, sodium, and potassium contents of these and all other vessels were not significantly changed in the hypertensive rabbits. The maximum response to norepinephrine in the ear artery, a representative vessel from the hypertensive part of the rabbit, was increased, whhereas the sensitivity of this vessel to norepinephrine expressed as the ED50 did not alter with changes in the arterial blood pressure. In contrast, the thickness and the maximum response to norepinephrine of the saphenous artery, representative of vessels distal to the ligature (normotensive vessels) and of the saphenous and cephalic veins were unaltered. The sensitivity as indicated by the norepinephrine ED50 of the veins, but not of the saphenous artery, increased with a rise in carotid artery blood pressure. These results suggest that the increased responsiveness to norepinephrine of arteries proximal to the ligature is due to changes in muscle mass and that the increased responsiveness of the veins is due to increased sensitivity to norepinephrine.