Steroids (aldosterone and testosterone) and peptides of cerebral origin (angiotensin II and the tachykinins) control the salt intake of the rat. They arouse or suppress the behavior and they produce lifelong enhancements of NaCl intake. Need-induced salt intake (salt appetite or salt hunger), which is the consequence of sodium deficiency, is aroused by a synergy within the brain of cerebral angiotensin II and aldosterone. And prior episodes of sodium depletion produce enhancements of subsequent salt appetites, but only if the prior depletions were accompanied by angiotensin II and aldosterone action. Need-free salt intake, which occurs daily when the rat is in positive sodium balance is also enhanced by prior activations of angiotensin II and aldosterone. Both need-induced and need-free salt intake are suppressed by intracranial tachykinins. Nonmammalian tachykinins (eledoisin, physalaemin, kassinin) are both antidipsogenic and antinatriorexigenic, but amino-senktide, an analog of the mammalian tachykinin substance P with selective affinity for the NK 3 receptor, appears to be a selective antinatriorexigenic agent, and could provide a rational therapy for chronic over-consumption of salt.