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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.
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-propyl-L-arginine (PLA) (B). Vessels
were pre-incubated with PLA (10–5 mol l–1)
for approximately 10 min prior to being pre-constricted with endothelin-1
(ET-1; 10–8 mol l–1). At the point of
maximal vasoconstriction, nicotine (3x10–4 mol
l–1) was added. Note that the vasodilation is reduced in the
presence of PLA. (C) Mean response (% vasodilation) of nicotine on
pre-constricted dorsal aorta and intestinal vein in the in the presence of
(filled bars) and in the absence of PLA (open bars). Note that PLA
significantly reduced the nicotine-mediated dilation (dorsal aorta and
intestinal vein, P<0.05; *denotes significant difference;
N=5).
