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This study investigated vasodilator mechanisms in the dorsal aorta of the elephant fish, Callorhinchus milii, using anatomical and physiological approaches. Nitric oxide synthase could only be located in the perivascular nerve fibres and not the endothelium of the dorsal aorta, using NADPH histochemistry and immunohistochemistry. In vitro organ bath experiments demonstrated that a NO/soluble guanylyl cyclase (GC) system appeared to be absent in the vascular smooth muscle, since the NO donors SNP (10−4 mol l−1) and SIN-1 (10−5 mol l−1) were without effect. Nicotine (3 × 10−4 mol l−1) mediated a vasodilation that was not affected by ODQ (10−5 mol l−1), l-NNA (10−4 mol l−1), indomethacin (10−5 mol l−1), or removal of the endothelium. In contrast, the voltage-gated sodium channel inhibitor, tetrodotoxin (10−5 mol l−1), significantly decreased the dilation induced by nicotine, suggesting that it contained a neural component. Pre-incubation of the dorsal aorta with the calcitonin gene-related peptide (CGRP) receptor antagonist, CGRP8–37 (10−6 mol l−1) also caused a significant decrease in the nicotine-induced dilation. We propose that nicotine is mediating a neurally-derived vasodilation in the dorsal aorta that is independent of NO, prostaglandins and the endothelium, and partly mediated by CGRP. [ABSTRACT FROM AUTHOR]