Spinal cord noradrenergic neurons are activated in hypotension.

Although norepinephrine-containing nerve terminals in the spinal cord synapse in the vicinity of sympathetic preganglionic cells, their effect on sympathetic outflow has remained unclear. Since survival during hypotension necessitates sustaining maximal sympathetic activity, we used experimental hypotension as a physiological stimulus to determine whether such activity is associated with an increase or a decrease in spinal cord norepinephrine turnover. Male Sprague-Dawley rats (500 g) were anesthetized with chloralose and urethane and their left carotid arteries were cannulated for blood pressure measurements and blood removal. Control animals remained normotensive during the 1-h study period; hypotensive animals were bled to a 50 mm Hg systolic pressure. Catecholamine release, as indicated by methoxyhydroxyphenylethyleneglycol sulfate (MHPG-SO4) concentrations, was greater in spinal cords of hypotensive rats than in normotensive controls. Apparent catecholamine synthesis also increased: norepinephrine concentrations did not change even though those of MHPG-SO4 doubled and the accumulation of dihydroxyphenylalanine (in other animals pretreated with NSD 1015) also doubled. These studies show that catecholamine-containing neurons in the spinal cord are stimulated in hypotension, and suggest that they may function physiologically to increase sympathetic outflow and thus blood pressure.