Intrarenal administration of angiotensin II does not moderate afferent renal nerve mediated cardiovascular reflexes in the anaesthetized rabbit.

Abstract

Stimulation of the afferent renal nerves in the anaesthetized rabbit by acute reduction in renal perfusion pressure results in a neurally mediated, reflex increase in hindlimb vascular resistance. To determine whether exogenous angiotensin II moderates the reflex, the kidneys of anaesthetized rabbits were vascularly isolated and renal blood flow was occluded acutely, following intrarenal administration of vehicle (0.9% saline) or angiotensin II (0.5 ng), and the hindlimb vascular response was measured. Occlusion of renal blood flow resulted in similar, significant increases in femoral perfusion pressure of 39.7 +/- 7.1 mmHg after vehicle and 21.3 +/- 8.9 mmHg (P < 0.05, n = 6) after angiotensin II. The viability of the preparation following repeated episodes of renal blood flow occlusion was tested by a series of three rapid (2-3 min delay) occlusions and three delayed (30 min delay) occlusions. Femoral perfusion pressure rose by 43.1 +/- 10.7 mmHg (rapid, P < 0.05, n = 11) and 64.4 +/- 12.3 mmHg (delayed, P < 0.05, n = 5) on the first occasion. On the second occasion, the rapid occlusion did not result in a significant increase in femoral perfusion pressure (29.1 +/- 8.1 mmHg), but the delayed group did (54.6 +/- 22.4 mmHg, P < 0.05). On the third occasion, neither group showed a significant change (20.9 +/- 16.3 and 30.8 +/- 13.5 mmHg). These data suggest that exogenous angiotensin II does not moderate the afferent renal nerve reflex. The decline in hindlimb response following rapid serial occlusion may be attributed to a diminution of an intermediary substance(s) at the nerve receptor site.