SUMMARY The abdominal aorta above the renal arteries was partially constricted or sham-constricted in rats age 6 weeks that had had adrenal demeduilation at age 4 weeks and guanethidine injections over Weeks 2-4 after birth to produce peripheral sympathectomy (S rats), and in sham-sympathectomized sbamdemedullated control rats (SS rats). Plasma noreplnephrine and epinephrine levels were reduced by 94-96% in S rats. Arterial pressures were also reduced by 30% in S rats, which, nevertheless, had hearts and aortas of normal size respective to body weight. With aortic coarctation, femoral arterial pressures did not increase but carotid pressures rose by 18-25% (p < 0.01). Expressed in terms of body weight, heart weights increased 75% and 50% (p < 0.001) and weights of eh* thoracic portion of the aorta Increased 58% and 37% (p < 0.05) with coarctation in SS and S rats, respectively. In SS rats there was also a rise in weight (26%) of the normotensive abdominal portion of the aorta (p < 0.01); in contrast, this was not true in S rats. In both SS and S rats, wall water contents of thoracic aorta, abdominal aorta, and thoracic vena cava increased by 3-8% with coarctation (p < 0.02). The normal size of heart and aorta in S rats, despite lower arterial pressures, suggests that factors other than pressure and sympathoadrenergic stimuli influence cardiovascular growth in young rats. The increased weight of the abdominal aorta in coarcted SS rats suggests that vascular wall hypertrophy in hypertension does not require elevated intravascular pressures. Increases in heart and thoracic aortic weight with coarctation in S rats suggest that cardiovascular hypertrophy may occur in the virtual absence of sympathoadrenergic stimuli. However, in the absence of both pressure and catecholamine influences, vascular hypertrophy apparently does not occur. Finally, these studies provide evidence for vascular wall “waterlogging” in coarctation hypertension in rats not attributable to elevated levels of intravascular pressure and occurring despite the virtual absence of sympathoadrenergic influences. These findings support the hypothesis that humoral factors are involved in vascular wall “waterlogging” in hypertension.