The aim of this study was to characterize the receptor subtype involved in cardiac effects of prostanoids. For this purpose we determined in neonatal and adult rat cardiomyocytes effects of prostanoids on inositol phosphate (InsP)-formation (assessed as accumulation of total [(3)H]-InsP's in myo-[(3)H]-inositol pre-labelled cells) and on rate of protein synthesis (assessed as [(3)H]-phenylalanine incorporation), and on contractile force in left ventricular strips of the rat heart. For comparison, effects of prostanoids on InsP-formation and contractile force were determined in rat thoracic aorta, a classical TP-receptor containing tissue. Prostanoid increased InsP-formation and rate of protein synthesis in neonatal as well as adult rat cardiomyocytes; the order of potency was in neonatal (PGF(2alpha)>PGD(2)> or =PGE(2)> or =U 46619>PGE(1)) and adult (PGF(2alpha)>PGD(2)> or =PGE(2)>U 46619) rat cardiomyocytes well comparable. Moreover, in electrically driven left ventricular strips PGF(2alpha) caused positive inotropic effects (pD(2) 7.5) whereas U 46619 (up to 1 microM) was uneffective. In contrast, in rat thoracic aorta U 46619 was about 100 times more potent than PGF(2alpha) in increasing InsP-formation and contractile force. The TP-receptor antagonist SQ 29548 only weakly antagonized prostanoid-induced increases in rate of protein synthesis (pK(B) about 6) in rat cardiomyocytes but was very potent (pK(B) about 8-9) in antagonizing prostanoid-induced increases in InsP-formation and contractile force in rat aorta. We conclude that, in cardiomyocytes of neonatal and adult rats, the prostanoid-receptor mediating increases in InsP-formation and rate of protein synthesis is a FP-receptor. Moreover, stimulation of these cardiac FP-receptors can mediate increases in contractile force.