In this study, we investigated the cardiovascular effects of four tachykinins in the anaesthetized toad, Bufo marinus. The potencies were compared of the amphibian peptides ranakinin and physalaemin and the mammalian peptide substance P, all of which interact preferentially with tachykinin NK-1 receptors. Neurokinin B, which is found in both mammals and amphibians, was also tested. All tachykinins produced dose-dependent decreases in arterial blood pressure. Ranakinin caused significantly greater falls in blood pressure than substance P, and the response was of longer duration. Both ranakinin and physalaemin were significantly more potent at decreasing blood pressure than neurokinin B. The NK-3 receptor selective agonist, senktide, caused no change in blood pressure. No tachykinin, at doses up to 10 nmole/kg, produced effects on baseline heart rate or affected the ability of the vagus nerves to slow the heart. A non-peptide NK-1 receptor antagonist, CP96,345 (in the dose range 10(-10)-5 x 10(-7) moles/kg) had no effect on the depressor action of ranakinin or substance P. It is concluded that amphibian tachykinins cause depressor effects via an NK-1-like receptor which differs substantially from its mammalian counterpart.