Contribution of nitric oxide (NO) and prostacyclin (PGI2) to endothelium‐dependent relaxation of porcine brachial and femoral arteries

Limited literature exists describing the relative contribution of NO and/or PGI 2 to endothelium‐dependent relaxation in the brachial and femoral arteries of humans or animals. The purpose of this investigation was to test the hypothesis that NO and PGI 2 have similar relative contributions to endothelium‐dependent relaxation in brachial and femoral arteries of quadrupeds. To test this hypothesis brachial and femoral arteries were harvested from 11 female miniature Yucatan swine. In vitro assessments of vasorelaxation to increasing doses of endothelium‐dependent (acetylcholine and bradykinin) and –independent (sodium nitroprusside) vasodilators were performed in the presence and absence of N G ‐nitro‐L‐arginine methyl ester [300μM (L‐NAME)], indomethacin [5μM (INDO)], and L‐NAME + INDO in both arteries. Vasorelaxation responses to endothelium‐dependent vasodilators were significantly attenuated, compared to controls, in both brachial and femoral arteries exposed to L‐NAME or L‐NAME + INDO but not those exposed to INDO. However, the vasorelaxtion responses of brachial arteries to endothelium‐dependent vasodilators were significantly more sensitive to L‐NAME (25 ± 4, 25 ± 4%) than those of the femoral arteries (12 ± 2, 14 ± 1%). In addition, there were no significant effects of INDO, L‐NAME, or L‐NAME + INDO on endothelium‐independent vasorelaxation of either type of artery compared to control. These results suggest a greater NO release in brachial than femoral arteries and do not support our hypothesis. Supported by: RR 18276, AR 048523, HL 36088, HL 52490