Skeletal muscle vasodilatation during sympathoexcitation is not neurally mediated in humans

1. Evidence for the existence of sympathetic vasodilator nerves in human sk eletal muscle is controversial. Manoeuvres such its contralateral ischaemic handgripping to fatigue that cause vasoconstriction in the resting forearm evoke vasodilatation after local alpha-adrenergic receptor blockade, raisi ng the possibility that both constrictor and dilator fibres are present. Th e purpose of this study mas to determine whether this dilatation is neurall y mediated. 2. Ten subjects (3 women, 7 men) performed ischaemic handgripping to fatigu e before and after acute local anaesthetic block of the sympathetic nerves (stellate ganglion) innervating the contralateral (resting) upper extremity Forearm blood flow was measured with venous occlusion plethysmography in t he resting forearm. 3. In control studies there was forearm vasoconstriction during contralater al handgripping to fatigue. During contralateral handgripping after stellat e block, blood flow in the resting forearm increased from 6.1 +/- 0.7 to 18 .7 +/- 2.2 ml dl(-1) min(-1) (P < 0.05). Mean arterial pressure measured co ncurrently increased from similar to 90 to 130 mmHg and estimated vascular conductance rose from 6.5 +/- 0.7 to 14.0 +/- 1.5 units, indicating that mo st of the rise in forearm blood flow mas due to vasodilatation. 4. Brachial artery administration of beta-blockers (propranolol) and the ni tric oxide (NO) synthase inhibitorN(G)-monomethlyl-L-arginine (L-NMMA) afte r stellate block virtually eliminated all of the vasodilatation to contrala teral handgrip. 5. Since vasodilatation was seen after stellate block, our data suggest tha t sympathetic dilator nerves are not responsible for limb vasodilatation se en during sympathoexcitation evoked by contralateral ischaemic handgripping to fatigue. The results obtained with propranolol and L-NMMA suggest that beta-adrenergic mechanisms and local NO release contribute to the dilatatio n.