Angiotensin-II acts centrally to alter renal sympathetic nerve activity and the intrarenal renin-angiotensin system.

Study Objective: The aim was to evaluate the influence that centrally administered angiotensin-II has on the intrarenal renin-angiotensin system and renal sympathetic nerve activity.

Design: Renal responses to centrally administered angiotensin-II (10 micrograms) or saralasin (50 micrograms) were measured in anaesthetised rats. The right kidney was vascularly isolated (but neurally intact) and perfused with artificial plasma at either a constant pressure (13.3 kPa) or constant flow (600 microliters.min-1) and renal vascular resistance was measured. Renal perfusate was collected at 10 min intervals after central administration of peptides and intrarenal concentrations of noradrenaline and renin were determined.

Subjects: Adult female Sprague-Dawley rats (200-225 g) were used. Rats were given thermal (or sham) lesions of the medial basal forebrain (MBF) 24 h prior to renal perfusion studies.

Results: Sham lesioned animals: central administration of angiotensin-II caused an increase in renal vascular resistance and intrarenal noradrenaline concentration in both the constant pressure and constant flow renal perfusion models. Central administration of angiotensin-II increased intrarenal renin concentration in the constant pressure model, while it decreased intrarenal renin concentration in the constant flow model. These effects of intracerebroventricular angiotensin-II were blocked by the concomitant administration of saralasin. Saralasin had no agonist actions on the responses measured. Medial basal forebrain lesioned animals: baseline levels of intrarenal noradrenaline concentration in both the constant flow and constant pressure perfusion models were significantly reduced compared to sham lesioned rats. Baseline intrarenal renin concentration was increased relative to sham lesioned rats in the constant flow perfusion model, but decreased relative to sham lesioned rats in the constant pressure perfusion model. Lesions of the medial basal forebrain block responses to intracerebroventricular angiotensin-II in both models.

Conclusions: Angiotensin-II appears to act on neurones within the medial basal forebrain to increase renal sympathetic nerve activity. Renal nerve activity interacts with the prevailing intrarenal pressure to modulate the release of renin.