The effect of 'stress' on salt and water balance is largely determined by intrinsic renal factors supported by a series of inter-related neuro-humoral mechanisms which serve to enhance salt and water reabsorption and to maintain arterial pressure. As shown by acute hypovolaemic stress, the hormone response is characterized by increased renin-angiotensin production and associated hyperaldosteronism, which is further augmented by states of Na+ depletion. As well as increasing aldosterone secretion, angiotensin II has a direct renal effect to increase Na+ retention, and may stimulate both thirst and arginine vasopressin secretion. Additional support to volume homeostasis is provided by increased secretion of hypothalamic hormones (arginine vasopressin and corticotrophin releasing factor) and activation of the sympathetic nervous system, which further enhances renin secretion. These mechanisms, in restoring extracellular fluid volume and renal perfusion pressure, eventually diminish the stimuli to renin once normovolaemia is achieved. A variety of other acute 'stressors', not associated with major changes in ECF volume or hypotension, also stimulate adrenocortical hormones (cortisol and aldosterone), renin and arginine vasopressin. The biological significance of these changes is uncertain, but their brief duration make it unlikely that the responses contribute significantly to changes in salt or water balance. Atrial peptide hormones could also be important in ECF volume regulation. However, recent studies show little if any change in basal plasma atrial natriuretic peptide levels during acute hypovolaemic stress, whereas severe treadmill exercise (but not surgical stress or acute hypoglycaemia) stimulates venous levels in man. The relevance of these findings to the regulation of salt and water balance during stress clearly requires further study.