With the aim of studying the pathophysiological background of the "TUR syndrome", we gave six conscious ewes an intravenous infusion of 57 ml/kg of 1.5% glycine solution over 40 min. Isotonic saline infusions served as controls. Central haemodynamics were monitored. The plasma concentrations of protein, K, Na and vasopressin, and plasma osmolality were measured repeatedly for up to 4 h. The urinary excretions of Na, K and osmoles were also followed. Both infusions caused an elevation of the mean arterial pressure. With glycine, the pressure increased from 93 +/- 4 to 112 +/- 12 mmHg (12.4 +/- 0.5 to 14.9 +/- 1.6 kPa) (mean +/- s.d.). The pulmonary capillary wedge pressure increased from 7 +/- 3 to 16 +/- 3 mmHg (0.9 +/- 0.4 to 2.1 +/- 0.4 kPa) and remained slightly elevated. The central venous pressure rose from 2 +/- 3 to 11 +/- 3 mmHg (0.3 +/- 0.4 to 1.5 +/- 0.4 kPa) but returned to baseline within 30 min after the infusion. Infusion of glycine resulted in a decrease in the plasma Na concentration from 144 +/- 3 to 114 +/- 4 mmol/l. The plasma osmolality decreased from 290 +/- 2 to 280 +/- 1 mosmol/l, and remained low. There was a median 6-fold increase in plasma vasopressin concentration, while saline did not elicit vasopressin release. Despite the absence of electrolytes in glycine solution, the urinary excretion of sodium amounted to 106 +/- 40 mmol. We conclude that i.v. infusion of 1.5% glycine solution in sheep causes a transient circulatory strain and natriuresis. Moreover, a vasopressin-mediated reduction of maximal water excretion contributes to persisting hypoosmolality.