 TP receptor-independent agents that stimulate cells to activate protein kinases C or protein kinases A can also down-regulate TP in a process termed heterologous desensitization.For example, prostacyclin I2 (PGI2)-induced activation of its prostacyclin receptor (IP) and prostaglandin D2-induced activation of its prostaglandin DP1 receptor cause TP receptor desensitization by activating protein kinases A while prostaglandin F2alpha-induced activation of its prostaglandin F receptor and prostaglandin E2-induced activation of its prostaglandin EP1 receptor receptor desensitizes TP by activating protein kinases C. These desensitization responses serve to limit the action of receptor agonists as well as the overall extent of cell excitation.In addition to its ability to down-regulate TPα, the IP receptor activates cell signaling pathways that counteract those activated by TP.