Scorpion toxin of Androctonus australis garzonii induces neuropeptide Y release via bradykinin stimulation in rat atria and kidneys

The ability of scorpion toxins to produce hemodynamic alterations is well documented but all mediators implied in cardiovascular disturbances are not known. In the present investigation we studied the effect of North African Androctonus australis garzonii scorpion toxin on neuropeptide Y (NPY) release from rat atria and kidneys by a perifusion system in vitro. To further understand the mechanisms of the scorpion toxin action on NPY release, the effects of icatibant (HOE 140, a selective bradykinin-B2 receptor antagonist), tetrodotoxin (TTX, a sodium channel antagonist) and diltiazem (a calcium channel antagonist), and the effect of the scorpion toxin on bradykinin (BK, a potent vasorelaxant peptide of the kinin group) release were studied in both tissues. We showed that the scorpion toxin (10−6 M) increased the NPY release from both atria (35%) and kidneys (40%). This increase was significantly (p < 0.001) inhibited by HOE 140 (10−5 M). The scorpion toxin (10−6 M) enhanced BK secretion in both atria (52%) and kidneys (55%). Diltiazem (10−5 M) and TTX (10−5 M) decreased by 45-75% NPY levels induced by scorpion toxin in both organs. The results show that A. australis garzonii scorpion toxin stimulates NPY release from both rat atria and kidneys, and suggest that the toxin induces NPY release via BK stimulation through B2 receptors. This effect appears to involve calcium and sodium channel activation.