ANG II type 1 (AT₁) receptors respond to sustained exposure to ANG II by undergoing downregulation of absolute receptor numbers. It has been assumed previously that downregulation involves endocytosis. The present study hypothesized that AT₁ receptor downregulation occurs independently of receptor endocytosis or G protein coupling. Mutant AT₁ receptors with carboxy-terminal deletions internalized <5% of radioligand compared with 65% for wild-type AT₁ receptors. The truncated AT₁ receptors retained the ability to undergo downregulation. These data suggest the existence of an alternative pathway to AT₁ receptor degradation that does not require endocytosis, per se. Point mutations in either the second transmembrane region or second intracellular loop impaired G protein (G_q) coupling. These receptors exhibited a biphasic pattern of downregulation. The earliest phase of downregulation (0–2 h) was independent of coupling to G_q, but no additional downregulation was observed after 2 h of ANG II exposure in the receptors with impaired coupling to G_q. These data suggest that coupling to G_q is required for the later phase (2–24 h) of AT₁ receptor downregulation.