In response to both hemodynamic and neurohumoral changes, the cardiovascular system remodels and this process could contribute to end organ damage. The aim of this study was to determine the early in vivo interactions between 3 systems known to contribute to vascular hypertrophic remodeling, in conduit and resistance arteries. Exogenous angiotensin II, norepinephrine and endothelin 1 administration elevated protein synthesis in the aorta and in small mesenteric arteries. In small arteries, the effect of angiotensin II was blocked by angiotensin II type 1, α-adrenergic and endothelin receptor antagonists, while only the α-adrenergic and endothelin receptor antagonists inhibited the effect of norepinephrine. Moreover, only the endothelin receptor antagonist significantly blunted the effect of exogenous endothelin on protein synthesis. In the aorta, the stimulation of angiotensin II on protein synthesis was also inhibited by the 3 antagonists. However, only the α-adrenoceptor antagonist blunted the response to norepinephrine, and the 3 antagonists prevented the endothelin-induced elevation of protein synthesis. The blood pressure effects of the drugs did not correlate with their capacity to stimulate or inhibit vascular protein synthesis. In conclusion, interactions in the control of protein synthesis are heterogeneous along the vascular tree. In small arteries, the interaction is linear with endothelin as the downstream effector. In the aorta, the local sympathetic nervous system appears to control protein synthesis. The heterogeneity in downstream effectors should be considered in studies investigating signaling events related to protein synthesis, which is used as an early marker of hypertrophy.