Fig. 5. Tension recordings from the intestinal vein showing the vasodilatory effect of nicotine (A) and its effect in the presence of the soluble guanylyl cyclase (GC) inhibitor ODQ (B) and the NOS inhibitor, L-NNA (C). Vessels were pre-incubated with ODQ (10^–5 mol l^–1) or L-NNA (10^–4 mol l^–1) for approximately 10 minprior to being constricted with endothelin-1 (ET-1; 10^–8 mol l^–1). No response was observed following the addition of nicotine (3x10^–4 mol l^–1) or SNP (10^–4 mol l^–1) to vessels incubated with ODQ. In contrast, the vessel dilated following the addition of rat ANP (10^–8 mol l^–1), which mediates its effect through a particulate GC, indicating that nicotine mediates its vasodilatory effect through the soluble GC. Following maximal constriction in the vessel preincubated with L-NNA, nicotine (3x10^–4 mol l^–1) was administered, but no vasodilatory effect was observed. Following this, the NOS independent NO donor, SNP (10^–4 mol l^–1), was added to the vessels, resulting in a marked vasodilation, suggesting that nicotine stimulates the production of NO via NOS to mediate vasodilation. Similar results were observed in the dorsal aorta (N=5). For abbreviations, see List.