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Inducible nitric oxide synthase (iNOS) generates nitric oxide (NO), which is known to modulate signal transduction processes by nitrosylating protein thiols. However, NO can also react with superoxide anion to form the potent oxidant peroxynitrite. We examined the effects of NO on endotoxin-induced expression of guanylate cyclase (GC) in aorta and mesenteric arterial bed. Incubation of rat aortas with a GC inhibitor (l-NG-nitroarginine methyl ester), but not a non-specific cyclooxygenase inhibitor (meclofenamate), enhanced the expression of GC mRNA induced by endotoxin. We also found that NO itself could suppress endotoxin-stimulated GC activity in rat aortic smooth muscle cells. In contrast, NO suppressed only partially the stimulatory effect of 8-bromo-cyclic GMP on GC activity in endothelial cells. Similarly, NO suppressed by 50% the stimulatory effect of endotoxin on GC activity in rat mesenteric arterial bed. Consistent with the in vivo data, treatment of rat aortic smooth muscle cells with a GC inhibitor (l-NG-nitroarginine methyl ester) enhanced endotoxin-stimulated production of tumor necrosis factor-alpha, suggesting that inhibition of endogenous NO production may potentiate induction of pro-inflammatory cytokines by endotoxin. In summary, NO suppresses endotoxin-induced expression of GC and its activity in vascular tissues. This negative effect may be one of the adaptive mechanisms of the vascular system to endotoxin. However, induction of pro-inflammatory cytokines by endotoxin may overwhelm this protective effect.Q:
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