1 The hypotensive and vasorelaxant e ect of dioclein in resistance mesenteric arteries was studied in intact animals and isolated vessels, respectively. 2 In intact animals, initial bolus administration of dioclein (2.5 mg kg 71 ) produced transient hypotension accompanied by an increase in heart rate. Subsequent doses of dioclein (5 and 10 mg kg 71 ) produced hypotensive responses with no signi®cant change in heart rate. N G -nitro-Larginine methyl ester (L-NAME) did not a ect the hypotensive response. 3 In endothelium-containing or -denuded vessels pre-contracted with phenylephrine, dioclein (5 and 10 mg kg 71 produced a concentration-dependent vasorelaxation (IC 50 =0.3+0.06 and 1.6+0.6 mM, respectively) which was not changed by 10 mM indomethacin. L-NAME (300 mM) produced a shift to the right. 4 Dioclein was without e ect on contraction of vessels induced by physiological salt solution (PSS) containing 50 mM KCl and the concentration dependence of dioclein's e ect on phenylephrine induced contraction was shifted to the right in vessels bathed in PSS containing 25 mM KCl. 5 Tetraethylammonium (10 mM) and BaCl 2 (1 mM) increased the IC 50 for dioclein-induced vasorelaxation without a ecting the maximal response (E max ). Charybdotoxin (100 nM), 4-aminopyridine (1 mM) and iberiotoxin (100 nM) increased the IC 50 and reduced the E max . Apamin (1 mM) reduced the E max without a ecting the IC 50 . 6 Dioclein produced a hyperpolarization in smooth muscle of mesenteric arteries with or without endothelium (7.7+1.4 mV and 12.3+3.6 mV, respectively). 7 In conclusion dioclein lowered arterial pressure probably through a decrease in peripheral vascular resistance. The underling mechanism implicated in the vasorelaxant e ect of dioclein appears to be the opening of K Ca and Kv channels and subsequent membrane hyperpolarization.