To test whether or not adrenal sympathetic innervation is required for the adrenocortical response to small hemorrhage, awake dogs were studied after unilateral adrenal sympathetic denervation. Bilateral adrenal vein cannulas were placed chronically to permit measurement of cortisol, epinephrine, and norepinephrine secretion rates and adrenal blood flow simultaneously from the intact and the denervated adrenal. Plasma ACTH concentration was measured and the presentation rate of ACTH was calculated as the product of plasma ACTH concentration and adrenal plasma flow. Unilateral isolation of the sympathetic chain from the spinal cord at thoracic levels 9–12 (T9–12) had no effect on adrenal blood flow, on the presentation rate of ACTH, or on cortisol secretion after 10 mg/kg hemorrhage. However, thoracic levels 9–12 denervation prevented the secretory response of catecholamines to hemorrhage without lowering basal catecholamine secretion. Unilateral splanchnicotomy, the sectioning of the thoracic and upper lumbar splanchnic nerves, reduced adrenal blood flow and the presentation rate of ACTH, suppressed basal catecholamine secretion, and prevented the catecholamine response to hemorrhage. However, there was no reduction in the secretory response of cortisol to 10% or 20% hemorrhage. These findings suggest that in the absence of sympathetic innervation to the adrenal, increases in adrenal sensitivity to ACTH occur to offset decreased ACTH presentation rate resulting in a normal cortisol response to hemorrhage. However, adrenal sensitivity to exogenous ACTH was not increased in nonhemorrhaged dogs after unilateral splanchnicotomy. Thus, hemorrhage must activate a non-ACTH mechanism that is independent of sympathetic adrenal innervation to augment adrenal sensitivity to ACTH. Sympathetic innervation to the adrenal has profound effects on catecholamine secretion and on adrenal blood flow but is not required for the secretory response of cortisol to small hemorrhage.