Role of E-type prostaglandin receptor EP3 in the vasoconstrictor activity evoked by prostacyclin in thromboxane-prostanoid receptor deficient mice.

Prostacyclin, also termed as prostaglandin I₂ (PGI₂), evokes contraction in vessels with limited expression of the prostacyclin receptor. Although the thromboxane-prostanoid receptor (TP) is proposed to mediate such a response of PGI₂, other unknown receptor(s) might also be involved. TP knockout (TP^-/-) mice were thus designed and used to test the hypothesis. Vessels, which normally show contraction to PGI₂, were isolated for functional and biochemical analyses. Here, we showed that the contractile response evoked by PGI₂ was indeed only partially abolished in the abdominal aorta of TP^-/- mice. Interestingly, further antagonizing the E-type prostaglandin receptor EP3 removed the remaining contractile activity, resulting in relaxation evoked by PGI₂ in such vessels of TP^-/- mice. These results suggest that EP3 along with TP contributes to vasoconstrictor responses evoked by PGI₂, and hence imply a novel mechanism for endothelial cyclooxygenase metabolites (which consist mainly of PGI₂) in regulating vascular functions.

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