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The effects of apamin, a polypeptide isolated from bee venom, on different vasodilator mechanisms in the small and large intestines were studied in atropinized cats. In the large intestine vasodilatation in response to pelvic nerve stimulation was either abolished or markedly diminished by I.A. apamin. However, neither the contraction of colonic muscle which occurred under these conditions nor sympathetic vasoconstriction was significantly influenced by apamin, suggesting that the effect of the peptide was not a non-specific effect on nerves or vascular smooth muscle. In the small intestine it was observed that the nervous vasodilatation induced by transmural electrical field stimulation or mechanical mucosal stimulation was either diminished or abolished by apamin. Intestinal vasodilatation, caused by close I.A. infusions of 5-hydroxytryptamine (5-HT), was abolished by apamin. After giving apamin 5-HT infusions induced a vasoconstriction in five out of six experiments. Vasodilatation induced by vasoactive intestinal polypeptide (VIP) was not significantly affected by apamin. In a series of in vitro experiments on rat portal vein, dose-response curves of several putative intestinal neurotransmitters were determined in the presence and absence of apamin. The following substances were tested: VIP, substance P, bradykinin, 5-HT, ATP and adenosine. Apamin had no effect on the dose-response curves of any of these compounds. The results are discussed in relation to the possibility that apamin may act by blocking the release of a putative peptidergic transmitter from nerve terminals.