Abstract

Introduction

Materials & Methods

Results

Discussion & Conclusion

References

Discussion
Board

Nitric oxide is known to relax the contractile tone of arteries. Since NO has been reported to interact with K+ channels, the question of the role of membrane potential changes in the relaxation is raised. The aim of the present study was to investigate the mechanism of the relaxation evoked by the NO donor SNAP in the superior mesenteric artery of the rat. Results showed that in arteries stimulated by noradrenaline. in the presence of N-nitro-L-arginine and indomethacin the relaxation to SNAP was associated with a parallel inhibition of the depolarization, of the increase in [Ca2+]cyt and of the accumulation of inositol phosphates evoked by noradrenaline. SNAP effects were inhibited by the guanylate cyclase blocker ODQ but were unaffected by K+ channel blockers. In arteries contracted and depolarized by AlF4-, SNAP relaxed the contraction and repolarized membrane potential. In arteries depolarized by 40 mM KCl, the relaxation to SNAP was not associated with change in [Ca2+]cyt and membrane potential. These results indicate that in addition to its effect on the contractile machinery, NO interacts with an early step of the excitation-contraction coupling process activated by noradrenaline.

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Presentation Number SAghisdal0672
Keywords: NO, mesenteric artery, K channels, inositol phosphat, Calcium