Initial desensitization due to rapid phosphorylation of activated receptors by kinases, which increases affinity for arrestin. Arrestin prevents protein-receptor interaction and the receptor becomes dephosphorylated and inhibited from signaling. This is a sufficient and rapid form of termination of PAR signaling. Irreversibly activated PAR1 is internalized and terminated from further signaling by clathrin-mediated endocytosis and lysosome degradation, preventing replenishment at the cell surface.