Neurons intrinsic to arterioles initiate postcontraction vasodilation

Ganglion cells exist in muscle arterioles. To determine the role of these intrinsic neurons in postcontraction vasodilation, isolated dog gracilis muscles were studied. A single twitch elicited vasodilation, but no vasodilator metabolites appeared in the venous effluent. Contraction at 2/s lowered resistance within 1 s whereas dilator metabolites were not demonstrable in the effluent until 15-20 s. During contraction the magnitude and time course of vasodilation were the same during constant and variable flow, and at various values of PaO2 and PVO2. In contrast, resistance was strongly correlated with flow and PO2 during recovery. Some resting muscles were perfused with venous blood from contracting donors. The rate of metabolic vasodilation in recipient muscles was about 10 times less than the rate of vasodilation in the donors. Lidocaine and procaine blocked postcontraction vasodilation but did not influence postocclusion vasodilation, metabolic vasodialtion, or autoregulation. The degree of block was the same in acutely and chronically denervated muscles. The effect of local anesthetics could not be accounted for by properties of skeletal or vascular smooth muscles.

1) intrinsic neurons initiate postcontraction vasodilation; 2) metabolites account for sustained vasodilation during recovery.