SUMMARYThe aim of the present experiment was to investigate the relative contribution of nitric oxide produced in endothelial cells to functional and reactive hyperaemia in the hindlimb of anaesthetized cats. Cats (2-5-3.4 kg) were anaesthetized with alphadalone-alphalaxone, and breathed spontaneously following tracheotomy. Left hindlimb blood flow was measured with a flow probe and hyperaemia responses were monitored following 10 s occlusion of the left external iliac artery and during 20 min stimulation of the sciatic and femoral nerves at 3 Hz. This was repeated following nitric oxide synthase inhibition with NG-nitro-L-arginine methyl ester (L-NAME, 100 mg kg-', i.v.). Following L-NAME administration, baseline hindlimb blood flow and arterial blood pressure were restored by infusion of sodium nitroprusside (range, 0-3-2-25 ,ug kg-l min-', i.v.). Following arterial occlusion, L-NAME reduced the peak reactive hyperaemia (6-5 ± 0-8 vs. 4.5 + 1.0 ml min-' kg-', P <0.05) and blood flow repayment (9-9 + 2-3 vs.6-1 + 2-6 ml, P < 0-05) responses. In contrast, the total functional hyperaemia response during hindlimb contraction was not altered (264-7 + 68-2 vs. 264-4 + 62-8 ml kg-', n.s.). The results of the study suggest that the production of nitric oxide from endothelial cells does not contribute to functional hyperaemia in contracting skeletal muscle, but plays a large role in reactive hyperaemia. The results imply that flow-dependent dilatation of feed arteries is mediated by NO in reactive hyperaemia.

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