Norepinephrine (NE, 10<sup>–5.5</sup> M) exposure for 4 h induces tone augmentation and vasodilation impairment after its removal. These changes are believed to represent early stages of inward remodeling. The hypothesis was tested that adrenoceptors causing vasoconstriction are responsible for NE-induced maintenance of augmented tone and vasodilation impairment, and that other vasoconstrictors associated with in vivo inward remodeling, a condition in which the internal passive diameter of arterioles is reduced without changes in medial cross-sectional area, also induce these changes in isolated arterioles. α-Adrenoceptor blockade prevented tone augmentation and vasodilation impairment, while β-adrenoceptor blockade allowed NE to induce those changes plus inward remodeling. Endothelin-1 (10<sup>–8</sup> M) induced tone augmentation and vasodilation impairment. Angiotensin II (ANG-II, 10<sup>–7</sup> M) and platelet-derived growth factor (10 ng/ml) did not. ANG-II did not cause sustained vasoconstriction, but induced inward remodeling dependent on presence of myogenic tone and tyrosine phosphorylation. Thus, prolonged vasoconstriction is not required during ANG-II-induced inward remodeling, suggesting remodeling processes effected by different agonists vary, with tone augmentation and impaired vasodilation occurring when vasoconstriction is required. This stresses the dynamic structure of arterioles, with rapid remodeling possibly involving functional changes and changes in extracellular matrix, cellular attachments, and/or cytoskeletal structures.