Section of the lumbar sympathetic chain just proximal to a stimulating electrode most often results in a large increase in the neurogenic constrictor response to stimulation. The increase could not be accounted for by removal of sympathetic discharge present before section, or by an increase in vascular sensitivity to either exogenous or neurogenically released adrenergic amine. The increased neurogenic constriction is attributed to the removal of an inhibition present before nerve section. The inhibitory fibers are distributed over the classic sympathetic outflow and take origin at least in part at a supraspinal level. The inhibition is lost or markedly reduced by hypotension, spinal cord section, spinal anesthesia, section of the preganglionic sympathetics, or by section of the sinus and vagus nerves. The inhibition, lost by sinus and vagus nerve section or by induction of hypotension, can be restored by stimulation of the central ends of the cut nerves and by replacement of blood, respectively. It is concluded that the conventional pressoreceptor reflexes act to inhibit vasoconstrictor tone, at least in part, at a site in the vasoconstrictor pathway peripheral to the spinal cord.