We have demonstrated recently that the luminal concentration of ATP in the S₂ region of the proximal tubule is considerably greater than that in the glomerular filtrate, suggesting ATP secretion into the lumen (Shirley et al. 2005a). Other studies have indicated that luminal nucleotides inhibit tubular transport (e.g. Bailey, 2004; Shirley et al. 2005b). It has been proposed that ATP release into the lumen might increase under ischaemic conditions, thereby helping to protect the tubular epithelium by inhibiting energy-consuming transport processes (Leipziger, 2003). In the present study we have assessed whether partial renal ischaemia following haemorrhagic hypotension leads to altered intraluminal ATP concentrations. Male Sprague-Dawley rats were anaesthetised (sodium thiopentone, 100mg kg^-1, I.P.) and prepared surgically for micropuncture of the left kidney. During a 1h control period, collections were made from mid-proximal convoluted tubules, each lasting 4 min. All tubular fluid samples were deposited in ice-cold water and frozen, to halt ATP degradation; 6-10 such collections were pooled from each animal. After the control period, eight rats were subjected to an arterial blood loss of 15 ml kg^-1 body weight; 30 min later, further collections were made from mid-proximal convoluted tubules (experimental period; 1h). Eight rats acted as time controls. All animals were killed humanely at the end of the experiment. ATP concentrations were determined using the luciferin-luciferase enzyme reaction. Mean arterial blood pressure (MABP) did not change significantly in the time-control animals. In rats subjected to haemorrhage, MABP was 112 ± 4 mmHg (mean ± S.E.M.) during the control period, fell to 42 ± 3 mmHg immediately after bleeding, and recovered partially to 92 ± 2 mmHg during the experimental period (both post-haemorrhage values significantly lower than the control values; P<0.001, ANOVA and Student-Newman-Keuls test). In time-control animals, proximal tubular ATP concentrations were 120 ± 15 nmol l^-1 during the control period and 125 ± 17 nmol l^-1 during the experimental period (NS, paired t test, P = 0.63). Corresponding values in bled rats were 120 ± 22 and 153 ± 38 nmol l^-1 (NS, P = 0.41). Although the possibility of altered ATP metabolism cannot be excluded, these data argue against a major change in proximal tubular secretion of ATP during haemorrhagic hypotension.