Effects of the diadenosine polyphosphates P(1),P(3)-diadenosine triphosphate (Ap3A), P(1),P(4)-diadenosine tetraphosphate (Ap4A), P(1),P(5)-diadenosine pentaphosphate (Ap5A) and P(1), P(6)-diadenosine hexaphosphate (Ap6A) and of adenosine, ATP, ADP, AMP, UTP on smooth muscle cells from porcine aorta were examined. Membrane voltages and cellular conductances were measured in the slow whole cell configuration of the patch clamp technique. All four diadenosine polyphosphates, adenosine, AMP and ADP predominantly hyperpolarized membrane voltages with only occasional transient initial depolarizations whereas ATP and UTP led to sustained depolarizations. All four diadenosine polyphosphates increased cellular conductances. The effects of Ap5A on membrane voltages were almost completely inhibited by the putative P2-purinoceptor antagonist pyridoxal-phosphate-6-azophenyl-2',4'-disulphonic acid (PPADS, 10 micromol/l) and only partially reduced by the putative A(2)-purinoceptor antagonist 3,7-dimethyl-1-propragyl-xanthine (DMPX, 10 micromol/l) or the Ap4A-receptor antagonist diinosine pentaphosphate (Ip5I, 10 micromol/l). The adenosine-induced hyperpolarization was partially reduced by the putative A(1)-purinoceptor antagonist 8-cyclopentyl-1,3-dipropargylxanthine (DPCPX, 0.1 micromol/l) or by DMPX while PPADS or Ip5I were without effects. Ap5A-induced hyperpolarizations were inhibited by Ba(2+) and clotrimazole but not by glibenclamide. We conclude that diadenosine polyphosphates activate predominantly a Ca(2+)-dependent K(+)-conductance in smooth muscle cells obtained from porcine aorta most likely mediated via P2Y-purinoceptors and possibly partially also by Ap4A receptors.