Rat small intestine was continuously perfused for up to 3 h with two different concentrations of sodium deoxycholate (4 and 8 mM) or with sodium ricinoleate (6 mM). The 4-mM bile salt solution produced a secretion that developed to a maximal rate within 3 h, whereas the maximal rate was reached within 1 h with the 8-mM bile salt solution. Hexamethonium, a ganglionic blocker, and lidocaine, a local anesthetic, always reduced the net fluid secretion to approximately zero irrespective of the rate of bile-salt-induced secretion, the concentration of the bile salt, or the perfusion time. Fluid secretion induced by sodium ricinoleate was, like the bile-salt-induced secretion, markedly inhibited by hexamethonium and lidocaine but not by atropine. It is concluded that the rate of secretion induced by the bile salt is related to the monomer concentration of free bile salt molecules in close proximity to or within the intestinal epithelium. The intestinal fluid secretion is mainly due to stimulation of an active secretory process via an activation of enteric nerves. Sodium ricinoleate evokes secretion via similar nervous reflex mechanisms.