1. The present study set out to explore the importance of angiotensin (Ang)II in the brain in allowing the somatosensory system to cause a reflex renal nerve-mediated reduction in renal sodium and water excretion. 2. In chloralose-urethane-anaesthetized rats receiving saline i.c.v. (2 microL + 1 microL/h), the administration of capsaicin (0.5 mg, s.c.) increased blood pressure by 14% (P < 0.001) and, while renal perfusion pressure was regulated at an unchanged level, neither renal blood flow (RBF) nor glomerular filtration rate was changed. However, urine flow and absolute and fractional sodium excretion was reduced between 29 and 38% (P<0.05-0.01). All variables had returned to control levels 30 min later. 3. The administration of captopril (40 microg + 20 microg/h i.c.v.) decreased blood pressure and sodium excretion by 6 and 17%, respectively (both P < 0.05). Under these conditions, capsaicin s.c. increased blood pressure by 9% (P<0.05); however, with renal perfusion pressure regulated at a constant level, neither renal haemodynamics nor water nor sodium excretion were changed. 4. A final group of animals received AngII (100 ng + 50 ng/h) concomitantly with captopril i.c.v., which increased blood pressure, RBF and urine flow, absolute and fractional sodium excretions by 8 (P < 0.05), 22 (P < 0.001 ) and 52-149% (P < 0.05-0.01), respectively. Capsaicin given s.c. under these conditions increased blood pressure by 6% (P < 0.05) and, while renal perfusion pressure was maintained at an unchanged value and renal haemodynamics remained constant, urine flow and absolute and fractional sodium excretion were reduced by 35-38% (all P < 0.05). 5. These data show that for the somatosensory system to induce a reflex increase in renal sympathetic nerve activity sufficient to cause an antinatriuresis and antidiuresis, the presence of AngII is necessary in the brain. How AngII exerts this facilitatory action within the central nervous system remains to be investigated.