THE EFFECT OF N-G-NITRO-L-ARGININE METHYL-ESTER UPON HINDLIMB BLOOD-FLOW RESPONSES TO MUSCLE-CONTRACTION IN THE ANESTHETIZED CAT

The aim of the present experiment was to investigate the relative cont ribution of nitric oxide produced in endothelial cells to functional a nd reactive hyperaemia in the hindlimb of anaesthetized cats. Cats (2. 5-3.4 kg) were anaesthetized with alphadalone-alphalaxone, and breathe d spontaneously following tracheotomy. Left hindlimb blood flow was me asured with a flow probe and hyperaemia responses were monitored follo wing 10 s occlusion of the left external iliac artery and during 20 mi n stimulation of the sciatic and femoral nerves at 3 Hz. This was repe ated following nitric oxide synthase inhibition with N-G-nitro-L-argin ine methyl ester (L-NAME, 100 mg kg(-1), i.v.). Following L-NAME admin istration, baseline hindlimb blood flow and arterial blood pressure we re restored by infusion of sodium nitroprusside (range, 0.3-2.25 mu g kg(-1) min(-1), i.v.). Following arterial occlusion, L-NAME reduced th e peak reactive hyperaemia (6.5 +/- 8 vs. 4.5 +/- 1.0 ml min(-1) kg(-1 ), 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 respons e during hindlimb contraction was not altered (264.7 +/- 68.2 vs. 264. 4 +/- 62.8 ml kg(-1), 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-depende nt dilatation of feed arteries is mediated by NO in reactive hyperaemi a.