The effect of NG-nitro-L-arginine methyl ester upon hindlimb blood flow responses to muscle contraction in the anaesthetized cat

Cardiovascular and Metabolism Department, ZENECA Pharmaceuticals, Mereside, Macclesfield, Cheshire, UK.
Experimental Physiology (Impact Factor: 2.67). 04/1995; 80(2):237-47. DOI: 10.1113/expphysiol.1995.sp003843
Source: PubMed


The 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-1, 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 micrograms kg-1 min-1, I.V.). Following arterial occlusion, L-NAME reduced the peak reactive hyperaemia (6.5 +/- 0.8 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 response 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-dependent dilatation of feed arteries is mediated by NO in reactive hyperaemia.

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    • "Indeed, L-NAME reduced baseline hindlimb blood flow by 45% in anaesthetized cats and attenuated the hyperaemia evoked by twitch contractions. However, when the baseline blood flow was restored with the NO donor sodium nitroprusside (SNP), the hyperaemia during muscle contraction was fully restored (Poucher, 1995). These results suggested that synthesis of NO is not necessary for the vasodilatation that accompanied muscle contraction, but that it is NO dependent. "
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