Abstract

Introduction

Materials & Methods

Results

Discussion & Conclusion

References

Discussion
Board

The contributions of nitric oxide (NO), prostacyclin (PGI2) and endothelium-derived hyperpolarizing factor (EDHF) to cerebral vasorelaxation appear to depend on different species. However, the mechanisms still remain elusive. The present study was undertaken to compare systematically their contributions to acetylcholine (ACh)- induced relaxation of the middle cerebral arteries isolated from rabbit (RMCA) and guinea-pig (GPMCA). In RMCA, ACh-induced relaxation was sensitive to either indomethacin (Ind, 10 然) or NG-nitro-L-arginine (L-NNA; 100 然) and abolished by their combination. In the presence of Ind, relaxation to ACh in RMCA was inhibited by charybdotoxin (CTX; 0.1 然) and ODQ (10 然). In the presence of L-NNA, relaxation to ACh was reduced by CTX and SQ-22536 (10 然). In contrast, ACh-induced relaxation of GPMCA was not abolished by L-NNA plus Ind. This L-NNA/Ind insensitive relaxation was inhibited by iberiotoxin (0.1 然), completely blocked by external high K+ PSS, CTX or clotrimazole (1 然). These results indicate the contributions of NO, PGI2 and EDHF to endothelium-dependent vaso- relaxation vary in a species- dependent fashion: 1) NO and PGI2 are involved in the relaxation of RMCA, 2) NO and EDHF are involved in the relaxation of GPMCA and EDHF in this vessel may be a cytochrome P450- derived metabolite.

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Presentation Number SAdong0185
Keywords: Cerebral artery, NO, PGI2, EDHF, Species differenc