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1. Male cats were anaesthetized with alphaxalone-alphadolone and breathed spontaneously following tracheotomy, Using coloured microspheres, muscle blood flow was measured at rest and during two periods of contraction elicited by simultaneous stimulation of the left sciatic and femoral nerves at 3 Hz for 10 min. In one group, the hindlimb blood flow was allowed to increase during muscle contraction and in another group the perfusion of the hindlimb was limited by a stenosis on the left external iliac artery. 2. In the absence of flow restriction, soleus muscle blood flow increased from 18.9 +/- 3.8 to 30.4 +/- 3.3 ml min-1 (100 g tissue)-1 (n = 6; P < 0.02) and gastrocnemius muscle blood flow increased from 24.8 +/- 5.9 to 61.6 +/- 12.8 ml min-1 (100 g tissue)-1 (n = 6; P < 0.01) during contraction. The bradykinin (BK) antagonists HOE 140 (1 mg kg-1, i.v.) did not affect the response in either the soleus (37.7 +/- 7.3 ml min-1 (100 g tissue)-1; n = 6; n.s.) or the gastrocnemius (62.9 +/- 7.9 ml min-1 (100 g tissue)-1; n = 6; n.s.) muscles. 3. In the stenosis group, soleus muscle blood flow increased from 9.8 +/- 2.3 to 22.9 +/- 4.9 ml min-1 (100 g tissue)-1 (n = 6; P < 0.01) and gastrocnemius muscle blood flow increased from 15.8 +/ 3.4 to 36.4 +/- 5.5 ml min-1 (100 g tissue)-1 (n = 6; P < 0.01) during contraction. Following administration of HOE 140, functional hyperaemia in the soleus muscle was unaffected (blood flow, 17.8 +/- 2.2 ml min-1 (100 g tissue)-1, n = 6; n.s.) white blood flow in the gastrocnemius muscle was reduced to 21.8 +/- 6.0 ml min-1 (100 g tissue)-1 (n = 6; P < 0.05). 4. The results show that BK does not contribute ot functional hyperaemia associated with twitch contraction at 3 Hz when blood flow is unrestricted, but may contribute up to 40% of the vasodilation of predominantly glycolytic muscle groups such as the gastrocnemius when flow is restricted. BK plays no role in hyperaemia associated with twitch contraction of oxidative muscle groups such as the soleus.

1. The present study was designed to investigate the contribution of the A(2A) adenosine receptor subtype in the functional hyperaemia response during muscle contraction. 2. In cats anaesthetized with sodium pentobarbitone and breathing spontaneously following tracheotomy, the left sciatic and femoral nerves were electrically stimulated at 3 Hz for 20 min to induce muscle contraction, and hindlimb blood flow was measured with a flow probe. The contribution of the A(2A) adenosine receptor subtype was assessed using ZM 241385, a potent and selective A(2A) adenosine receptor antagonist. 3. In a control group, the muscle isometric tension measured in the extensor digitorum longus-tibialis anterior muscle group was 6.64 +/- 0.66 kg (100 g muscle mass)(-1) and hindlimb vascular conductance was 0.22 +/- 0.03 ml mmHg(-1)(kg body mass)(-1) at 20 min of contraction. Administration of vehicle did not affect these parameters upon a second contraction period: 6.31 +/- 0.61 kg (100 g muscle mass)(-1) and 0.23 +/- 0.03 ml mmHg(-1) (kg body mass)(-1), respectively. Total hindlimb conductance during contraction was unaffected (5.5 +/- 3.7% decrease). 4. ZM 241385 (1.0 mg kg(-1)) did not alter the amount of force produced by the muscle at 20 min of contraction. Hindlimb conductance response was reduced by 27.1 +/- 4.8% following the A(2A) selective adenosine receptor antagonist, similar to that observed with the non-selective antagonist 8-phenyltheophylline. 5. These results show that adenosine acting at the A(2A) subtype receptor can contribute up to 30% of the functional hyperaemia response in the hindlimb of anaesthetized cats.

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.