Prostaglandin F 2α (PGF 2α) is produced during myocardial inflammation and many of the insults that trigger contractile dysfunction also activate prostaglandin synthesis and production. However, although PGF 2α plays a significant role in the cardiac response to inflammation, the effect of this particular compound on the heart was largely studied at the cellular level and probably no due attention was paid to the effect of PGF 2α on the whole heart contractility. Therefore, in the present study we have investigated the effect of PGF 2α on isolated right ventricle of the rat heart. PGF 2α (1 nM–1 μM) induced concentration-dependent decrease of the amplitude of contractions of the ventricular muscle. Real time RT-PCR has revealed that prostaglandin FP receptors are expressed in the rat myocardium and the level of expression was similar to those of creatine kinase and adenylate kinase, which are proteins abundantly present in the heart. An antagonist of FP receptors, PGF 2α dimetilamide (10 nM), abolished negative inotropic effect induced by PGF 2α. To examine the possibility that PGF 2α could activate non-FP prostaglandin receptor, we have measured the level of expression of all known prostaglandin receptors in the rat heart. These experiments have shown that the order of expression of prostaglandin receptors in the rat heart is FP ≫ EP1 = TP > EP4 > EP3 > DP = IP. Based on the obtained results we conclude that PGF 2α induces negative inotropic effect on rat heart by activating FP prostaglandin receptors. This effect of PGF 2α could contribute to cardiac dysfunction in conditions of systemic and myocardial inflammation.