In vitro experiments in a microvascular myograph were designed in order to characterize the receptor subtypes and the mechanisms underlying the contractions induced by neuropeptide Y (NPY) in rat coronary small arteries. The rank order of potency for NPY-receptor agonist-induced increases in tension in endothelium-intact preparations was polypeptide Y (PYY)> NPY > or = [Leu31Pro34]NPY, while NPY(13-36) only induced small contractions at the highest concentration applied. The selective neuropeptide Y1 receptor antagonist, BIBP 3226, caused rightward shifts in the concentration-response curves for NPY and the slope of the Schild plot was not significantly different from unity. The pA2 value for BIBP 3226 against NPY was 7.88+/-0.15 (n = 6). We have earlier shown that endothelial cell removal does not change the contractile responses induced by NPY, but indomethacin (3 x 10(-6) M) significantly reduced the contractions induced by the peptide. In contrast, the thromboxane receptor antagonist, SQ29548, which abolished the contractions induced by the thromboxane analogue, U46619, did not change the concentration-response curves for NPY. In conclusion, the present study suggests that Y1 receptors mediate NPY-induced contractions in rat coronary resistance arteries, and that a non-thromboxane prostanoid is involved in the contractile mechanism.