The homeostasis of body fluid traditionally is viewed as involving the regulation of its osmolality and of blood volume. However, the control of thirst is more complex than can be described in a two-factor model, and consideration of plasma sodium concentration and of arterial blood pressure also must be included in the discussion. This review is organized around those four variables and focuses on the seven distinct signals that appear to influence water intake in rats. These signals include four that are excitatory for thirst: increased plasma osmolality detected by cerebral osmoreceptors, decreased blood volume presumably detected by cardiac stretch receptors, increased circulating levels of angiotensin II detected by angiotensin II receptors in the subfornical organ, and increased gastric sodium load apparently detected by putative sodium receptors in the abdominal viscera. There also appear to be three signals that inhibit thirst: decreased plasma osmolality detected by cerebral osmoreceptors, increased arterial blood pressure detected by arterial baroreceptors, and increased gastric water load apparently detected by putative sodium receptors in the abdominal viscera.