The in vivo mechanisms whereby systemic α- and β-adrenergic stimulation exert opposing effects on renal water excretion are reviewed. An extrarenal mechanism is suggested since the effect of intravenous infusion of norepinephrine or isoproterenol on water excretion cannot be mimicked by the intrarenal administration of these agents. A role of vasopressin is implicated since neither man nor dog without a pituitary source of vasopressin demonstrate the same effect of catecholamines on water excretion as observed in intact man and dog. Evidence also is presented that systemic α- and β-adrenergic stimulation affect vasopressin release primarily by altering baroreceptor tone. The potential role of the autonomic nervous system in mediating other nonosmotic stimuli for vasopressin is discussed.