Neural control of skeletal muscle small arteries in the cat

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We hypothetized that activation of sympathetic cholinergic nerves to skeletal muscle causes a dilation of small arteries (internal diameter, 100-500mum). The aim of this study was 1) to study the vascular site at which the cholinergic vasodilation occurs during stimulation of posterior hypothalamus in anesthetized cats, and 2) to examine if endothelium-derived relaxing factor, nitric oxide, plays a role in cholinergic vasodilation. Femoral blood flow velocity (FBV) was measured with a Doppler flow probe. The distal caudal femoral artery has descending branches that supply the triceps surae muscle. Using and X-ray TV angiography, the distal caudal femoral artery (>500mum) and small arteries (100-500mum) in the triceps surae muscle was visualized by i.a. injecting a contrast medium. Arterial pressure, FBV,and femoral vascular conductance rose 15<plus-minus>8mmHg (mean<plus-minus>SE), 146<plus-minus>25%, and 139<plus-minus>25% during hypothalamic stimulation. The internal diameter of the distal caudal femoral artery did not alter during stimulation but the blood flow velocity was increased. In contrast, the internal diameter of small arteries in the triceps surae muscle increased 55<plus-minus>3% during hypothalamic stimulation, which was abolished by atropine or by cutting the sciatic nerve. The increase in internal diameter was blunted by a synthesis inhibitor of nitric oxide. It is concluded that stimulation of sympathetic cholinergic nerves to skeletal muscle causes a dilation of small arteries with internal diameter of 100-500mum, which is partly mediated by nit