Abstract
The ability of the prostacyclin (IP) receptor agonist cicaprost to activate G s-, G q/11- and G i-mediated cell signalling pathways has been examined in Chinese hamster ovary (CHO) cells and human embryonic kidney 293 (HEK 293) cells expressing the cloned human (hIP) or mouse (mIP) prostacyclin receptor, and compared with data from NG108-15 and SK-N-SH cells that endogenously express rat/mouse and human IP receptors, respectively. Cicaprost stimulated [ 3H]cyclic AMP production with EC 50 values of 1.5–22 nM, and stimulated [ 3H]inositol phosphate production (EC 50 values 49–457 nM) in all but the SK-N-SH cells. Cicaprost failed to inhibit forskolin-stimulated [ 3H]cyclic AMP production in any of these cell lines. Therefore, although both human and mouse IP receptors couple to G s and G q/11-mediated signalling pathways in a cell type-dependent manner, we could find no evidence for IP receptor coupling to G i.
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