Ganglion cells were found in arterioles of gracilis muscles of dogs 2 wk after complete extrinsic denervation. We tested the possibility that they function in active sympathetic vasodilation (SVD) induced in isolated gracilis muscles by hypothalamic stimulation. To this end various drugs were injected into the gracilis perfusate. (Drugs did not reach the systemic circulation, and exerted their effects within the gracilis itself). C6 had no effect. Submaximal doses of atropine or l-hyoscyamine delayed and slowed SVD; higher doses blocked completely. d-Hyoscyamine did not change SVD or acetylcholine vasodilation, but when administered prior to l-hyoscyamine, threshold for blockade of SVD by the l-isomer increased 10,000-fold. Blockade by l-hyoscyamine of acetylcholine vasodilation was unaltered by d-hyoscyamine. Eserine partly blocked SVD, but enhanced and prolonged acetylcholine vasodilation. The foregoing and certain features of the time course of SVD are interpreted to mean that: a) atropine blocks SVD at muscarinic sites on peripheral ganglion cells; b) transmission at the ganglion cells depends on slow excitatory postsynaptic potentials; c) the final mediator of SVD at the vascular muscle cell is unknown.